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Procyanidin B-2 Extracted from Apples Grows Hair in Clinical Trials of Male Pattern Baldness
In this study, the researchers concluded that procyanidin B-2 acts to diminish protein kinase C isozymes, which play an important role in the hair growth cycle.
Procyanidin B-2 seems to promote hair growth by downregulating PKC in both the anagen (active growth phase) and telogen (resting phase) of the hair follicle. When the anagen phase is prolonged, and the telogen phase is shortened, increased hair growth results.
Apple Chemical Grows Hair in Clinical Trials- Procyanidin B-2 Hair Growth Formula
......
Procyanidin B-2, extracted from apples, promotes hair growth: a laboratory study
Abstract
Background: We have previously reported that several selective protein kinase C (PKC) inhibitors, including procyanidin B-2, promote hair epithelial cell growth and stimulate anagen induction.
Objectives: We discuss the hypothesis that the hair-growing activity of procyanidin B-2 is related to its downregulation or inhibition of translocation of PKC isozymes in hair epithelial cells.
Methods: We examined the effect of procyanidin B-2 on the expression of PKC isozymes in cultured murine hair epithelial cells as well as PKC isozyme localization in murine dorsal skin at different stages in the hair cycle.
Results: We observed that procyanidin B-2 reduces the expression of PKC-alpha, -betaI, -betaII and -eta in cultured murine hair epithelial cells and also inhibits the translocation of these isozymes to the particulate fraction of hair epithelial cells. Our immunohistochemical analyses demonstrated that PKC-alpha, -betaI, -betaII and -eta are specifically expressed in the outer root sheaths of both anagen and telogen hair follicles. The hair matrix at the anagen stage showed no positive staining for these PKC isozymes. Moderate to intense staining for PKC-betaI and -betaII in the epidermis and hair follicles was observed in a telogen-specific manner; however, expression of PKC-alpha and -eta during the telogen stage was not conspicuous. Gö 6976, an inhibitor of calcium-dependent (conventional) PKC, proved to promote hair epithelial cell growth.
Conclusions: These results suggest that PKC isozymes, especially PKC-betaI and -betaII, play an important role in hair cycle progression and that the hair-growing mechanisms of procyanidin B-2 are at least partially related to its downregulation of PKC isozymes or its inhibition of translocation of PKC isozymes to the particulate fraction of hair epithelial cells.
Procyanidin B-2, extracted from apples, promotes hair growth: a laboratory study - PubMed
......
Procyanadin B2 - A Hair Growth Stimulant that protects the follicle from perifollicular fibrosis
What is it?
Procyanadin B-2 is an active ingredient found in Biotin Shampoo & Conditioner, Spark and Spark Plus.
Procyanidin B-2
Procyanidin B-2 is a polyphenol compound identified in apples which acts as a hair-growing factor. A kind of (proanthocyanidins and condensed tannins), one of the types of polyphenols and. It is also a strong antioxidant with many medical applications to date.
Is it safe? Are there side effects?
Isolated procyanidin B-2 to a purity exceeding 94% from apple juice and subjected it to a series of toxicological studies (Takahashi et al., 1999b). Results confirm the safety of topical application of procyanidin B-2 to human skin.
Effects on Hair loss
Acts as a protein kinase C (PKC) inhibitor, this molecules have been proved to stimulate (anagen phase) and to promote hair epithelial cell growth as (A.KAMIMURA AND T.TAKAHASHI) demonstrated back in 2001. The level of efficacy of 1 % procyanidin B-2 is concluded to compare favorably with minoxidil and finasteride therapy. In the procyanidin B-2 group, the increase in number of total hairs in the designated area (0.5 em square = 0.25 cml ) after the e-month trial was 6.68 ± 5.5 3 (mean ± SD)/0.25 cm2 , whereas in the placebo control group, the increase in number of total hair s was 0.0 8 ± 4.56 (mean ± SD)/0.25 cm2 (Table 2). It is calculated th at the increased number of total hairs in the designated area of procyanidin B-2 group subjects after the 6-month trial was significantly greater than that of the placebo control group subjects
Structure & Synthesis
20 kl of apple juice (Malus pumila Miller var) eluted and evaporated to produce 233 g of a dry solid.
Mechanisms of Action
The main mechanism of action of procyanidin B-2 is implied by its intensive growth-promoting action on hair epithelial cells (Takahashi et al., 1999a). The intensive anti-oxidative activity of procyanidin B-2 may be a significant contributor to its effects. The relation between male pattern baldness and inflammation has been pointed out by several researchers. It has been reported that lymphocytic inflammation was observed around hair follicles biopsied from patients showing male pattern baldness (Sueki et aI., 1999; Jaworsky et aI., 1992). Young et a1. (1991) also reported that the ratio of subjects showing inflammation of the scalp was 100 % in subjects with male pattern baldness, whereas the ratio was 66 % in non-balding subjects. Procyanidins are known to show the effect of decreasing inflammation due to their anti-oxidative properties (Haslam, 1996) and by their protease inhibiting action (Tixier et al., 1984). Therefore, it is supposed that the suppression of inflammation mediated by procyanidin B-2 returns the scalp to a healthy condition, consequently leading to a cure for baldness
Procyanadin B2 - A Hair Growth Stimulant that protects the follicle from perifollicular fibrosis
.............
Procyanidin B-2, extracted from apples, promote hair growth: A laboratory study
Abstract
We have previously reported that several selective protein kinase C (PKC) inhibitors, including procyanidin B-2, promote hair epithelial cell growth and stimulate anagen induction. We discuss the hypothesis that the hair-growing activity of procyanidin B-2 is related to its downregulation or inhibition of translocation of PKC isozymes in hair epithelial cells. We examined the effect of procyanidin B-2 on the expression of PKC isozymes in cultured murine hair epithelial cells as well as PKC isozyme localization in murine dorsal skin at different stages in the hair cycle. We observed that procyanidin B-2 reduces the expression of PKC-alpha, -betaI, -betaII and -eta in cultured murine hair epithelial cells and also inhibits the translocation of these isozymes to the particulate fraction of hair epithelial cells. Our immunohistochemical analyses demonstrated that PKC-alpha, -betaI, -betaII and -eta are specifically expressed in the outer root sheaths of both anagen and telogen hair follicles. The hair matrix at the anagen stage showed no positive staining for these PKC isozymes. Moderate to intense staining for PKC-betaI and -betaII in the epidermis and hair follicles was observed in a telogen-specific manner; however, expression of PKC-alpha and -eta during the telogen stage was not conspicuous. Gö 6976, an inhibitor of calcium-dependent (conventional) PKC, proved to promote hair epithelial cell growth. These results suggest that PKC isozymes, especially PKC-betaI and -betaII, play an important role in hair cycle progression and that the hair-growing mechanisms of procyanidin B-2 are at least partially related to its downregulation of PKC isozymes or its inhibition of translocation of PKC isozymes to the particulate fraction of hair epithelial cells.
Procyanidin B-2, extracted from apples, promote hair growth: A laboratory study | Request PDF
..........
Suppression of estrogen biosynthesis by procyanidin dimers in red wine and grape seeds - PubMed
.........
Bradykinin and angiotensin II: activation of protein kinase C in arterial smooth muscle
Abstract
The effects of bradykinin (BK) and angiotensin II (ANG II) were compared in cultured rat mesenteric arterial smooth muscle cells. BK and ANG II activated a phosphoinositide-specific phospholipase C, leading to the rapid release of [3H]inositol phosphates, an increase in intracellular calcium, and formation of sn-1,2-diacylglycerol (DAG). DAG formation was biphasic with a transient peak at 5 s followed by a sustained increase from 60 to 600 s. The BK-mediated increases in inositol triphosphate and DAG were dose dependent with half-maximal increases at concentrations of 5 and 2 nM, respectively. Both hormones were found to activate protein kinase C (PKC) as assessed by phosphorylation of the 68- to 72-kDa intracellular PKC substrate myristoylated alanine-rich C kinase substrate. However, despite similar phosphorylation of this substrate, only ANG II produced a significant increase in membrane-bound PKC activity. The mechanism accounting for the inability of BK to increase membrane-bound PKC activity is unclear. Our studies excluded differential translocation of PKC to the nuclear membrane, production of an inhibitor of membrane-bound PKC activity, and expression of BK and ANG II receptors on different cells as the mechanism. Vascular smooth muscle cells were found to express at least four different PKC isozymes: alpha, delta, zeta, and a faint band for epsilon. All of the isozymes except zeta-PKC were translocated by treatment with the phorbol ester 4 beta-phorbol 12-myristate 13-acetate. However, neither ANG II nor BK produced significant translocation of any measured isozyme; therefore, we could not exclude the possibility that ANG II and BK activate different isozymes of PKC. Both hormones were found to have a similar small and inconsistent effect in stimulating [3H]thymidine incorporation. These observations demonstrate that BK and ANG II have similar biochemical effects on vascular smooth muscle cells and imply that, in selected vessels, the vasodilatory effects of BK mediated by the endothelium may be partially counterbalanced by a vasoconstrictor effect on the underlying vascular smooth muscle cells.
https://journals.physiology.org/doi/abs/10.1152/ajpcell.1994.266.5.C1406?journalCode=ajpcell
…..
Protein kinase C regulates vascular calcification via cytoskeleton reorganization and osteogenic signaling
Abstract
Vascular calcification is an active cell-mediated process that reduces elasticity of blood vessels and increases blood pressure. Until now, the molecular basis of vascular calcification has not been fully understood. We previously reported that microtubule disturbances mediate vascular calcification. Here, we found that protein kinase C (PKC) signaling acted as a novel coordinator between cytoskeletal changes and hyperphosphatemia-induced vascular calcification. Phosphorylation and expression of both PKCα and PKCδ decreased during inorganic phosphate (Pi)-induced vascular smooth muscle cell (VSMC) calcification. Knockdown of PKC isoforms by short interfering RNA as well as PKC inactivation by Go6976 or rottlerin treatment revealed that specific inhibition of PKCα and PKCδ accelerated Pi-induced calcification both in VSMCs and ex vivo aorta culture through upregulation of osteogenic signaling. Additionally, inhibition of PKCα and PKCδ induced disassembly of microtubule and actin, respectively. In summary, our results indicate that cytoskeleton perturbation via PKCα and PKCδ inactivation potentiates vascular calcification through osteogenic signal induction.
Protein kinase C regulates vascular calcification via cytoskeleton reorganization and osteogenic signaling - PubMed
………
Protein kinase C promotes cardiac fibrosis and heart failure by modulating galectin-3 expression
Highlights
•We examined the signaling pathway for PKC-α in heart failure.
•Activation of the PKC pathway stimulates galectin-3 expression.
•Inhibition of galectin-3 blocks PKC-stimulated collagen production.
•Both PKC-α and galectin-3 are upregulated in experimental heart failure.
•Angiotensin II by activation of the PKC pathway promotes galectin-3 expression.
Conclusions
Numerous animal and human studies have demonstrated that PKC-α activation or an increase in PKC-α expression is associated with HF and that inhibition of PKC-α is cardioprotective. In this study, we report the new finding that PKC-α regulates galectin-3, another crucial mediator of cardiac remodeling, cardiac fibrosis and HF, independent of contractility regulation. The distinction of the current study is the reconciliation of these two important but different kinds of HF mediators and the discovery that they work synergistically in the process of HF development. We thus propose that with the onset of heart disease, augmented PKC-α increases galectin-3 expression which subsequently promotes cardiac fibrosis and HF. We also found that the action of Ang II, a well-known stimulator of cardiac hypertrophy and remodeling, may be mediated, in part, by the activation of the PKC–galectin-3 pathway.
Protein kinase C promotes cardiac fibrosis and heart failure by modulating galectin-3 expression
.....
Galectin-3 (Gal3) is a member of the lectin family and has a molecular weight of about 30 kDa. Like all galectins, gal3 also includes amino acids that bind to β-galactosides [11]. Gal3 is responsible for a number of processes including apoptosis, cell cycle, cell growth, cell activation, and cell adhesion. Moreover, it has been shown to have a major role in heart failure, cancer, inflammation, fibrosis, stroke, diabetes, obesity, and atherosclerosis. In addition, it has been reported to play a key role in impaired follicular growth in patients with PCOS
Investigation of galectin-3, lipocalin 2, retinol binding protein (RBP), small dense low-density lipoprotein (sdLDL) in patients with hirsutism
……
Galectins are highly expressed in epithelial cells and immune cells. In skin, they can be detected in keratinocytes, melanocytes, dendritic cells, macrophages, and T cells. Galectins are present outside and inside the cells and thus may exhibit different functions through extracellular and intracellular actions. Galectins can be involved in the pathogenesis of inflammatory skin diseases by affecting growth, apoptosis, maturation, activation, and motility of keratinocytes and immune cells. Expression of galectins may change depending on the cellular status, such as proliferation and activation. For example, galectin-3 expression is upregulated in T cells but downregulated in dendritic cells when these cells are activated. Furthermore, their expression may also change under pathological conditions. Understanding the function of each galectin in keratinocytes and different immune cell types may reveal how galectins contribute to the pathogenesis of immune-mediated skin diseases.
Galectins and cutaneous immunity
........
Serum galectin-3 levels in women with PCOS
Abstract
Aim: Galectin-3 (Gal-3) plays a role in modulation of adiposity, glucose hemostasis and inflammation. The association between Gal-3 and the polycystic ovary syndrome (PCOS), is not investigated. We aimed to evaluate galectin-3 levels in serum and their relation with hyperandrogenism and insulin resistance (IR) in women with polycystic ovary syndrome (PCOS) and in control subjects.
Materials and methods: 56 women with PCOS were enrolled along with a control group of 41 healthy women, matched for age and body mass index. We measured hormonal and metabolic parameters, as well as the serum galectin-3 concentration of each participant. We estimated the IR according to the homeostasis model assessment-insulin resistance (HOMA-IR).
Results: Women with PCOS had higher levels of serum Gal-3 compared to healthy individuals (3,588.77 ± 1,566.94 vs 2,491.33 ± 812.04, P < 0.001). Serum Gal-3 levels were correlated with progesterone (r = 0.241, P = 0.025), hirsutism score (r = 0.296, P = 0.006), insulin (r = 0.479, P = 0.028), HOMA-IR (r = 0.514, P = 0.017), dehydroepiandrosterone sulfate (r = 0.246, P = 0.022), testosterone (r = 0.252, P = 0.019), and free testosterone (r = 0.306, P = 0.004).
Conclusion: Galectin-3 levels are higher in patients with PCOS, and there is a positive correlation between galectin-3 level and IR, androgen levels and hirsutismus scores. Gal-3 may be a new mediator of PCOS via IR, hyperandrogenism.
Serum galectin-3 levels in women with PCOS - PubMed
- The increase in number of total hairs and terminal hairs in the procyanidin B-2 group subjects was significantly greater than controls
- 78.9% of subjects showed an increased mean value of hair diameter
- "Procyanidin B-2 therapy shows promise as a cure for male pattern baldness."
In this study, the researchers concluded that procyanidin B-2 acts to diminish protein kinase C isozymes, which play an important role in the hair growth cycle.
Procyanidin B-2 seems to promote hair growth by downregulating PKC in both the anagen (active growth phase) and telogen (resting phase) of the hair follicle. When the anagen phase is prolonged, and the telogen phase is shortened, increased hair growth results.
Apple Chemical Grows Hair in Clinical Trials- Procyanidin B-2 Hair Growth Formula
......
Procyanidin B-2, extracted from apples, promotes hair growth: a laboratory study
Abstract
Background: We have previously reported that several selective protein kinase C (PKC) inhibitors, including procyanidin B-2, promote hair epithelial cell growth and stimulate anagen induction.
Objectives: We discuss the hypothesis that the hair-growing activity of procyanidin B-2 is related to its downregulation or inhibition of translocation of PKC isozymes in hair epithelial cells.
Methods: We examined the effect of procyanidin B-2 on the expression of PKC isozymes in cultured murine hair epithelial cells as well as PKC isozyme localization in murine dorsal skin at different stages in the hair cycle.
Results: We observed that procyanidin B-2 reduces the expression of PKC-alpha, -betaI, -betaII and -eta in cultured murine hair epithelial cells and also inhibits the translocation of these isozymes to the particulate fraction of hair epithelial cells. Our immunohistochemical analyses demonstrated that PKC-alpha, -betaI, -betaII and -eta are specifically expressed in the outer root sheaths of both anagen and telogen hair follicles. The hair matrix at the anagen stage showed no positive staining for these PKC isozymes. Moderate to intense staining for PKC-betaI and -betaII in the epidermis and hair follicles was observed in a telogen-specific manner; however, expression of PKC-alpha and -eta during the telogen stage was not conspicuous. Gö 6976, an inhibitor of calcium-dependent (conventional) PKC, proved to promote hair epithelial cell growth.
Conclusions: These results suggest that PKC isozymes, especially PKC-betaI and -betaII, play an important role in hair cycle progression and that the hair-growing mechanisms of procyanidin B-2 are at least partially related to its downregulation of PKC isozymes or its inhibition of translocation of PKC isozymes to the particulate fraction of hair epithelial cells.
Procyanidin B-2, extracted from apples, promotes hair growth: a laboratory study - PubMed
......
Procyanadin B2 - A Hair Growth Stimulant that protects the follicle from perifollicular fibrosis
What is it?
Procyanadin B-2 is an active ingredient found in Biotin Shampoo & Conditioner, Spark and Spark Plus.
Procyanidin B-2
Procyanidin B-2 is a polyphenol compound identified in apples which acts as a hair-growing factor. A kind of (proanthocyanidins and condensed tannins), one of the types of polyphenols and. It is also a strong antioxidant with many medical applications to date.
Is it safe? Are there side effects?
Isolated procyanidin B-2 to a purity exceeding 94% from apple juice and subjected it to a series of toxicological studies (Takahashi et al., 1999b). Results confirm the safety of topical application of procyanidin B-2 to human skin.
Effects on Hair loss
Acts as a protein kinase C (PKC) inhibitor, this molecules have been proved to stimulate (anagen phase) and to promote hair epithelial cell growth as (A.KAMIMURA AND T.TAKAHASHI) demonstrated back in 2001. The level of efficacy of 1 % procyanidin B-2 is concluded to compare favorably with minoxidil and finasteride therapy. In the procyanidin B-2 group, the increase in number of total hairs in the designated area (0.5 em square = 0.25 cml ) after the e-month trial was 6.68 ± 5.5 3 (mean ± SD)/0.25 cm2 , whereas in the placebo control group, the increase in number of total hair s was 0.0 8 ± 4.56 (mean ± SD)/0.25 cm2 (Table 2). It is calculated th at the increased number of total hairs in the designated area of procyanidin B-2 group subjects after the 6-month trial was significantly greater than that of the placebo control group subjects
Structure & Synthesis
20 kl of apple juice (Malus pumila Miller var) eluted and evaporated to produce 233 g of a dry solid.
Mechanisms of Action
The main mechanism of action of procyanidin B-2 is implied by its intensive growth-promoting action on hair epithelial cells (Takahashi et al., 1999a). The intensive anti-oxidative activity of procyanidin B-2 may be a significant contributor to its effects. The relation between male pattern baldness and inflammation has been pointed out by several researchers. It has been reported that lymphocytic inflammation was observed around hair follicles biopsied from patients showing male pattern baldness (Sueki et aI., 1999; Jaworsky et aI., 1992). Young et a1. (1991) also reported that the ratio of subjects showing inflammation of the scalp was 100 % in subjects with male pattern baldness, whereas the ratio was 66 % in non-balding subjects. Procyanidins are known to show the effect of decreasing inflammation due to their anti-oxidative properties (Haslam, 1996) and by their protease inhibiting action (Tixier et al., 1984). Therefore, it is supposed that the suppression of inflammation mediated by procyanidin B-2 returns the scalp to a healthy condition, consequently leading to a cure for baldness
Procyanadin B2 - A Hair Growth Stimulant that protects the follicle from perifollicular fibrosis
.............
Procyanidin B-2, extracted from apples, promote hair growth: A laboratory study
Abstract
We have previously reported that several selective protein kinase C (PKC) inhibitors, including procyanidin B-2, promote hair epithelial cell growth and stimulate anagen induction. We discuss the hypothesis that the hair-growing activity of procyanidin B-2 is related to its downregulation or inhibition of translocation of PKC isozymes in hair epithelial cells. We examined the effect of procyanidin B-2 on the expression of PKC isozymes in cultured murine hair epithelial cells as well as PKC isozyme localization in murine dorsal skin at different stages in the hair cycle. We observed that procyanidin B-2 reduces the expression of PKC-alpha, -betaI, -betaII and -eta in cultured murine hair epithelial cells and also inhibits the translocation of these isozymes to the particulate fraction of hair epithelial cells. Our immunohistochemical analyses demonstrated that PKC-alpha, -betaI, -betaII and -eta are specifically expressed in the outer root sheaths of both anagen and telogen hair follicles. The hair matrix at the anagen stage showed no positive staining for these PKC isozymes. Moderate to intense staining for PKC-betaI and -betaII in the epidermis and hair follicles was observed in a telogen-specific manner; however, expression of PKC-alpha and -eta during the telogen stage was not conspicuous. Gö 6976, an inhibitor of calcium-dependent (conventional) PKC, proved to promote hair epithelial cell growth. These results suggest that PKC isozymes, especially PKC-betaI and -betaII, play an important role in hair cycle progression and that the hair-growing mechanisms of procyanidin B-2 are at least partially related to its downregulation of PKC isozymes or its inhibition of translocation of PKC isozymes to the particulate fraction of hair epithelial cells.
Procyanidin B-2, extracted from apples, promote hair growth: A laboratory study | Request PDF
..........
Suppression of estrogen biosynthesis by procyanidin dimers in red wine and grape seeds
"The efficacy of these procyanidin B dimer compounds was then evaluated in an aromatase transfected MCF-7 breast cancer mouse model. The B dimer mixture was able to reduce androgen dependent tumor growth, indicating that procyanidin B dimers suppress in situ estrogen formation. This was done in collaboration with Dr. Rajeshwar Rao Tekmal at Emory University using a transgenic mouse model that over-expresses aromatase in the mammary tissues. Like the known specific aromatase inhibitor, Letrozole, the active B dimer fraction from red wine (administered by gavage) is a potent blocker of estrogen biosynthesis. When feed to the mice by gavage, it led not only to complete reduction and elimination of breast hyperplasia and other preneoplastic and neoplastic changes, but also affected other normal endocrine functions that are typical for estrogen deprivation."Suppression of estrogen biosynthesis by procyanidin dimers in red wine and grape seeds - PubMed
.........
Bradykinin and angiotensin II: activation of protein kinase C in arterial smooth muscle
Abstract
The effects of bradykinin (BK) and angiotensin II (ANG II) were compared in cultured rat mesenteric arterial smooth muscle cells. BK and ANG II activated a phosphoinositide-specific phospholipase C, leading to the rapid release of [3H]inositol phosphates, an increase in intracellular calcium, and formation of sn-1,2-diacylglycerol (DAG). DAG formation was biphasic with a transient peak at 5 s followed by a sustained increase from 60 to 600 s. The BK-mediated increases in inositol triphosphate and DAG were dose dependent with half-maximal increases at concentrations of 5 and 2 nM, respectively. Both hormones were found to activate protein kinase C (PKC) as assessed by phosphorylation of the 68- to 72-kDa intracellular PKC substrate myristoylated alanine-rich C kinase substrate. However, despite similar phosphorylation of this substrate, only ANG II produced a significant increase in membrane-bound PKC activity. The mechanism accounting for the inability of BK to increase membrane-bound PKC activity is unclear. Our studies excluded differential translocation of PKC to the nuclear membrane, production of an inhibitor of membrane-bound PKC activity, and expression of BK and ANG II receptors on different cells as the mechanism. Vascular smooth muscle cells were found to express at least four different PKC isozymes: alpha, delta, zeta, and a faint band for epsilon. All of the isozymes except zeta-PKC were translocated by treatment with the phorbol ester 4 beta-phorbol 12-myristate 13-acetate. However, neither ANG II nor BK produced significant translocation of any measured isozyme; therefore, we could not exclude the possibility that ANG II and BK activate different isozymes of PKC. Both hormones were found to have a similar small and inconsistent effect in stimulating [3H]thymidine incorporation. These observations demonstrate that BK and ANG II have similar biochemical effects on vascular smooth muscle cells and imply that, in selected vessels, the vasodilatory effects of BK mediated by the endothelium may be partially counterbalanced by a vasoconstrictor effect on the underlying vascular smooth muscle cells.
https://journals.physiology.org/doi/abs/10.1152/ajpcell.1994.266.5.C1406?journalCode=ajpcell
…..
Protein kinase C regulates vascular calcification via cytoskeleton reorganization and osteogenic signaling
Abstract
Vascular calcification is an active cell-mediated process that reduces elasticity of blood vessels and increases blood pressure. Until now, the molecular basis of vascular calcification has not been fully understood. We previously reported that microtubule disturbances mediate vascular calcification. Here, we found that protein kinase C (PKC) signaling acted as a novel coordinator between cytoskeletal changes and hyperphosphatemia-induced vascular calcification. Phosphorylation and expression of both PKCα and PKCδ decreased during inorganic phosphate (Pi)-induced vascular smooth muscle cell (VSMC) calcification. Knockdown of PKC isoforms by short interfering RNA as well as PKC inactivation by Go6976 or rottlerin treatment revealed that specific inhibition of PKCα and PKCδ accelerated Pi-induced calcification both in VSMCs and ex vivo aorta culture through upregulation of osteogenic signaling. Additionally, inhibition of PKCα and PKCδ induced disassembly of microtubule and actin, respectively. In summary, our results indicate that cytoskeleton perturbation via PKCα and PKCδ inactivation potentiates vascular calcification through osteogenic signal induction.
Protein kinase C regulates vascular calcification via cytoskeleton reorganization and osteogenic signaling - PubMed
………
Protein kinase C promotes cardiac fibrosis and heart failure by modulating galectin-3 expression
Highlights
•We examined the signaling pathway for PKC-α in heart failure.
•Activation of the PKC pathway stimulates galectin-3 expression.
•Inhibition of galectin-3 blocks PKC-stimulated collagen production.
•Both PKC-α and galectin-3 are upregulated in experimental heart failure.
•Angiotensin II by activation of the PKC pathway promotes galectin-3 expression.
Conclusions
Numerous animal and human studies have demonstrated that PKC-α activation or an increase in PKC-α expression is associated with HF and that inhibition of PKC-α is cardioprotective. In this study, we report the new finding that PKC-α regulates galectin-3, another crucial mediator of cardiac remodeling, cardiac fibrosis and HF, independent of contractility regulation. The distinction of the current study is the reconciliation of these two important but different kinds of HF mediators and the discovery that they work synergistically in the process of HF development. We thus propose that with the onset of heart disease, augmented PKC-α increases galectin-3 expression which subsequently promotes cardiac fibrosis and HF. We also found that the action of Ang II, a well-known stimulator of cardiac hypertrophy and remodeling, may be mediated, in part, by the activation of the PKC–galectin-3 pathway.
Protein kinase C promotes cardiac fibrosis and heart failure by modulating galectin-3 expression
.....
Galectin-3 (Gal3) is a member of the lectin family and has a molecular weight of about 30 kDa. Like all galectins, gal3 also includes amino acids that bind to β-galactosides [11]. Gal3 is responsible for a number of processes including apoptosis, cell cycle, cell growth, cell activation, and cell adhesion. Moreover, it has been shown to have a major role in heart failure, cancer, inflammation, fibrosis, stroke, diabetes, obesity, and atherosclerosis. In addition, it has been reported to play a key role in impaired follicular growth in patients with PCOS
Investigation of galectin-3, lipocalin 2, retinol binding protein (RBP), small dense low-density lipoprotein (sdLDL) in patients with hirsutism
……
Galectins are highly expressed in epithelial cells and immune cells. In skin, they can be detected in keratinocytes, melanocytes, dendritic cells, macrophages, and T cells. Galectins are present outside and inside the cells and thus may exhibit different functions through extracellular and intracellular actions. Galectins can be involved in the pathogenesis of inflammatory skin diseases by affecting growth, apoptosis, maturation, activation, and motility of keratinocytes and immune cells. Expression of galectins may change depending on the cellular status, such as proliferation and activation. For example, galectin-3 expression is upregulated in T cells but downregulated in dendritic cells when these cells are activated. Furthermore, their expression may also change under pathological conditions. Understanding the function of each galectin in keratinocytes and different immune cell types may reveal how galectins contribute to the pathogenesis of immune-mediated skin diseases.
Galectins and cutaneous immunity
........
Serum galectin-3 levels in women with PCOS
Abstract
Aim: Galectin-3 (Gal-3) plays a role in modulation of adiposity, glucose hemostasis and inflammation. The association between Gal-3 and the polycystic ovary syndrome (PCOS), is not investigated. We aimed to evaluate galectin-3 levels in serum and their relation with hyperandrogenism and insulin resistance (IR) in women with polycystic ovary syndrome (PCOS) and in control subjects.
Materials and methods: 56 women with PCOS were enrolled along with a control group of 41 healthy women, matched for age and body mass index. We measured hormonal and metabolic parameters, as well as the serum galectin-3 concentration of each participant. We estimated the IR according to the homeostasis model assessment-insulin resistance (HOMA-IR).
Results: Women with PCOS had higher levels of serum Gal-3 compared to healthy individuals (3,588.77 ± 1,566.94 vs 2,491.33 ± 812.04, P < 0.001). Serum Gal-3 levels were correlated with progesterone (r = 0.241, P = 0.025), hirsutism score (r = 0.296, P = 0.006), insulin (r = 0.479, P = 0.028), HOMA-IR (r = 0.514, P = 0.017), dehydroepiandrosterone sulfate (r = 0.246, P = 0.022), testosterone (r = 0.252, P = 0.019), and free testosterone (r = 0.306, P = 0.004).
Conclusion: Galectin-3 levels are higher in patients with PCOS, and there is a positive correlation between galectin-3 level and IR, androgen levels and hirsutismus scores. Gal-3 may be a new mediator of PCOS via IR, hyperandrogenism.
Serum galectin-3 levels in women with PCOS - PubMed
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