Hypoxia induces expression of connective tissue growth factor in scleroderma skin fib

[squeegee]

Hypoxia induces expression of connective tissue growth factor in scleroderma skin fibroblasts.

lin Exp Immunol. 2006 Nov;146(2):362-70.Hypoxia induces expression of connective tissue growth factor in scleroderma skin fibroblasts.

Hong KH, Yoo SA, Kang SS, Choi JJ, Kim WU, Cho CS.
Source

Department of Internal Medicine, Division of Rheumatology, School of Medicine, Catholic University of Korea, Seoul, Korea.

Abstract

Connective tissue growth factor (CTGF) plays a role in the fibrotic process of systemic sclerosis (SSc). Because hypoxia is associated with fibrosis in several profibrogenic conditions, we investigated whether CTGF expression in SSc fibroblasts is regulated by hypoxia. Dermal fibroblasts from patients with SSc and healthy controls were cultured in the presence of hypoxia or cobalt chloride (CoCl(2)), a chemical inducer of hypoxia-inducible factor (HIF)-1alpha. Expression of CTGF was evaluated by Northern and Western blot analyses. Dermal fibroblasts exposed to hypoxia (1% O(2)) or CoCl(2) (1-100 microM) enhanced expression of CTGF mRNA. Skin fibroblasts transfected with HIF-1alpha showed the increased levels of CTGF protein and mRNA, as well as nuclear staining of HIF-1alpha, which was enhanced further by treatment of CoCl(2). Simultaneous treatment of CoCl(2) and transforming growth factor (TGF)-beta additively increased CTGF mRNA in dermal fibroblasts. Interferon-gamma inhibited the TGF-beta-induced CTGF mRNA expression dose-dependently in dermal fibroblasts, but they failed to hamper the CoCl(2)-induced CTGF mRNA expression. In addition, CoCl(2) treatment increased nuclear factor (NF)-kappaB binding activity for CTGF mRNA, while decreasing IkappaBalpha expression in dermal fibroblasts. Our data suggest that hypoxia, caused possibly by microvascular alterations, up-regulates CTGF expression through the activation of HIF-1alpha in dermal fibroblasts of SSc patients, and thereby contributes to the progression of skin fibrosis.




http://www.ncbi.nlm.nih.gov/pubmed/17034590



-the lowest oxygen levels were found in the thickened fibrotic skin

http://books.google.ca/books?id=CHg...y#v=onepage&q=dermal fibrosis hypoxia&f=false

 

[dam]

ahh whats this in english lol, i use neogenic wich induces hypoxia.

 

[benjt]

In English: Avoid hypoxia, it speeds up the hairloss process by accelerating fibrosis.

 

[DoctorHouse]

Neogenic acts on STEM CELLS. I think its a different process than what this article is talking about.

 

[dam]

I have been using neogenic since last march only on my temple area wich is my problem spot. I apply it just under my hairline and all over my sides and bald temple area. What i noticed in the first month was small vellus hairs forming but can only see them under certain light in my mirror and i know for a fact they were not there before. I tried applying 5% minoxidil foam once a day and Neogenic at night hopefully to boost growth but in the first three weeks of applying minoxidil my vellus hairs disappeared. I then started applying Neogenic again without minoxidil and got the same results small vellus hairs growing again. This time i seem to have more but i still can only see them in certain lights in the mirror. I doubt if they will ever turn terminal but its doing something. Just thought i would share guys. I am gonna try a Neogenic for another month then try minoxidil on one side of my temple and Neogenic on the other side and see what happens. What Neogenic claims to do is to erase the sleep cycle and wake up dormant hair This is done because some stem cells thrive in a Hypoxic environment .

 

[IDW2BB]

http://www.ncbi.nlm.nih.gov/pubmed/24999590

Hypoxia-inducible factors regulate filaggrin expression and epidermal barrier function.
Wong WJ1, Richardson T2, Seykora JT3, Cotsarelis G3, Simon MC4.
Author information
Abstract
A functional epidermal skin barrier requires the formation of a cornified envelope from terminally differentiating keratinocytes. During this process, multiple genetic and environmental signals coordinately regulate protein expression and tissue differentiation. Here we describe a critical role for hypoxia-inducible factors (HIFs) in the regulation of filaggrin expression and skin barrier formation. Similar to other mammalian tissues, fetal epidermis in mice is normally O2 deprived. Simultaneous deletion of Hif1a and Hif2a in murine epidermis revealed defects in keratinocyte terminal differentiation and epidermal barrier formation. Mice lacking Hif1a and Hif2a in the epidermis exhibited dry flaky skin, impaired permeability barrier, and enhanced sensitivity to cutaneous allergens. These defects were correlated with stratum granulosum attenuation and reduced filaggrin expression. Hypoxic treatment of primary keratinocytes induced filaggrin (Flg) gene expression in a HIF1α- and HIF2α-dependent manner, suggesting that one mechanism by which Hif1a and Hif2a loss causes epidermal barrier defects in mice lies in Flg dysregulation. Therefore, low O2 tension is an essential component of the epidermal environment that contributes to skin development and function.

Is our balding hair actually casualties of a battle between the different layers or our skin?