Редактирование: COL7A1

Collagen alpha-1(VII) chain precursor (Long-chain collagen) (LC collagen)

==Publications==

{{medline-entry
|title=Biological Effects Induced by Specific Advanced Glycation End Products in the Reconstructed Skin Model of Aging.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/26309782
|abstract=Advanced glycation end products (AGEs) accumulate in the aging skin. To understand the biological effects of individual AGEs, skin reconstructed with collagen selectively enriched with N(ɛ)-(carboxymethyl)-lysine (CML), N(ɛ)-(carboxyethyl)-lysine ([[CEL]]), methylglyoxal hydroimidazolone (MG-H1), or pentosidine was studied. Immunohistochemistry revealed increased expression of α6 integrin at the dermal epidermal junction by [[CEL]] and CML (p<0.01). Laminin 5 was diminished by [[CEL]] and MG-H1 (p<0.05). Both CML and [[CEL]] induced a robust increase (p<0.01) in procollagen I. In the culture medium, IL-6, VEGF, and [[MMP1]] secretion were significantly decreased (p<0.05) by MG-H1. While both [[CEL]] and CML decreased [[MMP3]], only [[CEL]] decreased IL-6 and [[TIMP1]], while CML stimulated [[TIMP1]] synthesis significantly (p<0.05). mRNA expression studies using qPCR in the epidermis layer showed that [[CEL]] increased type 7 collagen ([[COL7A1]]), β1, and α6 integrin, while CML increased only [[COL7A1]] (p<0.05). MG-H1-modified collagen had no effect. Importantly, in the dermis layer, [[MMP3]] mRNA expression was increased by both CML and MG-H1. CML also significantly increased the mRNAs of [[MMP1]], [[TIMP1]], keratinocyte growth factor (KGF), IL-6, and monocyte chemoattractant protein 1 (MCP1) (p<0.05). Mixed effects were present in [[CEL]]-rich matrix. Minimally glycoxidized pentosidine-rich collagen suppressed most mRNAs of the genes studied (p<0.05) and decreased VEGF and increased MCP1 protein expression. Taken together, this model of the aging skin suggests that a combination of AGEs tends to counterbalance and thus minimizes the detrimental biological effects of individual AGEs. 

|keywords=* aging
* extracellular matrix
* glucose
* glycation
* methylglyoxal
* oxoaldehydes
|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4497626
}}