Elevation of intracellular calcium - Hair Loss

md_a

Member
Joined
Aug 31, 2015
Messages
366
„Magnesium and potassium are mainly intracellular ions, sodium and calcium are mainly extracellular ions. When cells are excited, stressed, or de-energized, they lose magnesium and potassium, and take up sodium and calcium. The mitochondria can bind a certain amount of calcium during stress, but accumulating calcium can reach a point at which it inactivates the mitochondria, forcing cells to increase their inefficient glycolytic energy production, producing an excess of lactic acid. Abnormal calcification begins in the mitochondria.

When cells are stressed or dying, they take up calcium, which tends to excite the cells at the same time that it inhibits their energy production, intensifying their stress. A cramp or a seizure is an example of uncontrolled cellular excitation. Prolonged excitation and stress contribute to tissue inflammation and fibrosis.

Gross calcification generally follows the fibrosis that is produced by inflammation.” Ray Peat

....

Pharmacological Activation of Thermo–Transient Receptor Potential Vanilloid 3 Channels Inhibits Hair Growth by Inducing Cell Death of Hair Follicle Outer Root Sheath

Abstract

Hair growth starts from hair follicles that reside in dermis, and abnormal hair growth is an early sign of hair follicle disease or systemic illness such as alopecia or hair loss.
Therefore, identifying a target critical for dysfunctional hair follicles is fundamental to alleviating dermatologic or systemic diseases with hair abnormalities. The warm temperature–activated Ca2+-permeable transient receptor potential vanilloid 3 (TRPV3) channel protein is abundantly expressed in the skin keratinocytes, and dysfunctional TRPV3 causes human congenital Olmsted syndrome, characterized by skin diseases and alopecia, indicating an important role for TRPV3 in hair follicle development and hair growth. To validate TRPV3 as a therapeutic target, we investigated the impact of pharmacological modulation of TRPV3 on hair growth using a combination of biochemical and cell biology, immunohistochemical, whole-cell patch clamp, RNA interference, and pharmacological approaches. We found that functional TRPV3 channel proteins are highly expressed in hair follicle outer root sheath (ORS) cells as detected by Western blot analysis, immunohistochemical staining, and electrophysiological techniques. Pharmacological activation of TRPV3 by agonist natural carvacrol induces cell death of ORS cells, and topical application of carvacrol to mouse dorsal skin also inhibits hair growth. Conversely, specific inhibition of TRPV3 by inhibitor natural forsythoside B and short-hairpin RNA reverses the cell death induced by carvacrol-mediated TRPV3 activation in human ORS cells. Furthermore, forsythoside B results in a significant reversal of hair growth inhibition induced by agonist carvacrol. Altogether, our findings demonstrate that TRPV3 channel is critical for regulation of hair growth, and inhibition of TRPV3 may represent a promising therapy for hair loss or hair follicle–related skin diseases.

Pharmacological Activation of Thermo–Transient Receptor Potential Vanilloid 3 Channels Inhibits Hair Growth by Inducing Cell Death of Hair Follicle Outer Root Sheath

...

Inhibition of the Warm Temperature–Activated Ca2+-Permeable Transient Receptor Potential Vanilloid TRPV3 Channel Attenuates Atopic Dermatitis​

A proposed mechanism underlying the temperature-sensitive Ca2+-permeable TRPV3 channel in the progressive pathology of AD. For overactive TRPV3-mediated inflammatory signaling, activation of TRPV3 by agonist carvacrol or gain-of-function mutations (G573S, G573C, W692G, and G573A) leads to an elevation of intracellular calcium. When Ca2+ in the cytoplasm increase, the phosphorylation of IκBα (inactivation) and p65 (activation) results in translocation of p65 to the nucleus in the skin keratinocytes, thus activating the nuclear factor-κB pathway for inducing the production and release of inflammatory factors aggravates the pathology of AD or skin inflammation. Inhibition of TRPV3 by natural osthole or silencing reduces the release of inflammatory factors. Topical inhibition of TRPV3 channel function may represent an effective prevention and management strategy for treatment of AD by alleviation of skin lesions, edema, and severe itching or other inflammatory skin diseases.

https://molpharm.aspetjournals.org/content/96/3/393/tab-figures-data

...

Hair-growth-stimulating effect of minoxidil is stimulation of PGE2 synthesis by activating prostaglandin-H synthase (PGHS)-1. Normally, Calcium influx normally enhances epidermal growth factors to inhibit hair growth. Minoxidil is converted to minoxidil sulfate, which is a potassium channel agonist and enhances potassium ion permeability, thus opposing the entry of calcium into cells. It also seems to have direct mitogenic effect on epidermal cells and also prolongs the survival time of keratinocytes [8].

2015.1-2. | Our Dermatology Online journal
 

dabdabdab

Member
Joined
May 28, 2020
Messages
106
„Magnesium and potassium are mainly intracellular ions, sodium and calcium are mainly extracellular ions. When cells are excited, stressed, or de-energized, they lose magnesium and potassium, and take up sodium and calcium. The mitochondria can bind a certain amount of calcium during stress, but accumulating calcium can reach a point at which it inactivates the mitochondria, forcing cells to increase their inefficient glycolytic energy production, producing an excess of lactic acid. Abnormal calcification begins in the mitochondria.
When cells are stressed or dying, they take up calcium, which tends to excite the cells at the same time that it inhibits their energy production, intensifying their stress. A cramp or a seizure is an example of uncontrolled cellular excitation. Prolonged excitation and stress contribute to tissue inflammation and fibrosis.
Gross calcification generally follows the fibrosis that is produced by inflammation.” Ray Peat
....
Pharmacological Activation of Thermo–Transient Receptor Potential Vanilloid 3 Channels Inhibits Hair Growth by Inducing Cell Death of Hair Follicle Outer Root Sheath
Abstract
Hair growth starts from hair follicles that reside in dermis, and abnormal hair growth is an early sign of hair follicle disease or systemic illness such as alopecia or hair loss.
Therefore, identifying a target critical for dysfunctional hair follicles is fundamental to alleviating dermatologic or systemic diseases with hair abnormalities. The warm temperature–activated Ca2+-permeable transient receptor potential vanilloid 3 (TRPV3) channel protein is abundantly expressed in the skin keratinocytes, and dysfunctional TRPV3 causes human congenital Olmsted syndrome, characterized by skin diseases and alopecia, indicating an important role for TRPV3 in hair follicle development and hair growth. To validate TRPV3 as a therapeutic target, we investigated the impact of pharmacological modulation of TRPV3 on hair growth using a combination of biochemical and cell biology, immunohistochemical, whole-cell patch clamp, RNA interference, and pharmacological approaches. We found that functional TRPV3 channel proteins are highly expressed in hair follicle outer root sheath (ORS) cells as detected by Western blot analysis, immunohistochemical staining, and electrophysiological techniques. Pharmacological activation of TRPV3 by agonist natural carvacrol induces cell death of ORS cells, and topical application of carvacrol to mouse dorsal skin also inhibits hair growth. Conversely, specific inhibition of TRPV3 by inhibitor natural forsythoside B and short-hairpin RNA reverses the cell death induced by carvacrol-mediated TRPV3 activation in human ORS cells. Furthermore, forsythoside B results in a significant reversal of hair growth inhibition induced by agonist carvacrol. Altogether, our findings demonstrate that TRPV3 channel is critical for regulation of hair growth, and inhibition of TRPV3 may represent a promising therapy for hair loss or hair follicle–related skin diseases.
Pharmacological Activation of Thermo–Transient Receptor Potential Vanilloid 3 Channels Inhibits Hair Growth by Inducing Cell Death of Hair Follicle Outer Root Sheath
...

Inhibition of the Warm Temperature–Activated Ca2+-Permeable Transient Receptor Potential Vanilloid TRPV3 Channel Attenuates Atopic Dermatitis​

A proposed mechanism underlying the temperature-sensitive Ca2+-permeable TRPV3 channel in the progressive pathology of AD. For overactive TRPV3-mediated inflammatory signaling, activation of TRPV3 by agonist carvacrol or gain-of-function mutations (G573S, G573C, W692G, and G573A) leads to an elevation of intracellular calcium. When Ca2+ in the cytoplasm increase, the phosphorylation of IκBα (inactivation) and p65 (activation) results in translocation of p65 to the nucleus in the skin keratinocytes, thus activating the nuclear factor-κB pathway for inducing the production and release of inflammatory factors aggravates the pathology of AD or skin inflammation. Inhibition of TRPV3 by natural osthole or silencing reduces the release of inflammatory factors. Topical inhibition of TRPV3 channel function may represent an effective prevention and management strategy for treatment of AD by alleviation of skin lesions, edema, and severe itching or other inflammatory skin diseases.
Inhibition of the Warm Temperature–Activated Ca2+-Permeable Transient Receptor Potential Vanilloid TRPV3 Channel Attenuates Atopic Dermatitis
...
Hair-growth-stimulating effect of minoxidil is stimulation of PGE2 synthesis by activating prostaglandin-H synthase (PGHS)-1. Normally, Calcium influx normally enhances epidermal growth factors to inhibit hair growth. Minoxidil is converted to minoxidil sulfate, which is a potassium channel agonist and enhances potassium ion permeability, thus opposing the entry of calcium into cells. It also seems to have direct mitogenic effect on epidermal cells and also prolongs the survival time of keratinocytes [8].
2015.1-2. | Our Dermatology Online journal
 

GorillaHead

Member
Joined
Oct 21, 2018
Messages
1,706
Location
USA
Does high extracellular calcium inhibit intracellular calcium? Or do we just need high levels of magnesium?
 
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