Background: Several of the characteristic clinical features of photoaged skin, including wrinkling, are thought to be dependent on changes in the dermal matrix brought about by chronic sun exposure. Such changes include reductions in collagens I, III and VII, an increase in elastotic material in the reticular dermis and a marked reduction in the microfibrillar glycoprotein fibrillin.
Objectives: To examine whether type VI collagen, a microfibrillar collagen necessary for cell-cell and cell-matrix communication, is affected by the photoageing process.
Methods: Six healthy volunteers with moderate to severe photoageing were enrolled into the study. Immunohistochemistry and in situ hybridization histochemistry were used to examine the levels of type VI collagen in photoprotected and photoaged sites.
Results: In photoprotected skin, type VI collagen was concentrated in the papillary dermis immediately below the dermal-epidermal junction, around blood vessels, hair follicles and glandular structures. The distribution of type VI collagen was unchanged in photoaged skin, although we observed an increase in the abundance of the alpha3 chain of collagen VI in the upper papillary dermis, at its junction with the dermal-epidermal junction (P < 0.05). No alterations were observed for any alpha chain at the mRNA level.
Conclusions: These studies suggest that chronic sun exposure (photoageing) has little or no effect on either the distribution, abundance or levels of expression of type VI collagen in human skin. Thus, type VI collagen, unlike other matrix components so far studied, appears to be relatively unaffected by the photoageing process.
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http://dx.doi.org/10.1046/j.1365-2133.2001.04012.x | DOI Listing |
Biochemistry
January 2025
Biomolecular Research Institute, Boise State University, 1910 University Drive, Boise, Idaho 83725, United States.
The amino-terminal domain of collagen α1(XI) plays a key role in controlling fibrillogenesis. However, the specific mechanisms through which various isoforms of collagen α1(XI) regulate this process are not fully understood. We measured the kinetics of collagen type I self-assembly in the presence of specific collagen α1(XI) isoforms.
View Article and Find Full Text PDFCirc Res
January 2025
Hypertension Research Laboratory, School of Biological Sciences (R.R.M., T.Z., E.D., L.X., A.B.-W., H.A.J., M.N., M.P., K.C.L., W.Q., J.A.O.D., F.Z.M.).
Background: Fermentation of dietary fiber by the gut microbiota leads to the production of metabolites called short-chain fatty acids, which lower blood pressure and exert cardioprotective effects. Short-chain fatty acids activate host signaling responses via the functionally redundant receptors GPR41 and GPR43, which are highly expressed by immune cells. Whether and how these receptors protect against hypertension or mediate the cardioprotective effects of dietary fiber remains unknown.
View Article and Find Full Text PDFCirc Res
January 2025
Institute for Cardiovascular and Metabolic Research, Health and Life Sciences Building, University of Reading, United Kingdom. (N.K., C.K., J.L.D., T.S., S.R., M.V.D.A., V.S., N.R., C.I.J., J.M.G.).
Basic Clin Pharmacol Toxicol
February 2025
Department of Pharmacology, Venkateshwara College of Pharmacy, Meerut, India.
Background: Rheumatoid arthritis (RA) is a long-term inflammatory autoimmune disease that damages cartilage and synovial membranes while also affecting bones and joints. The aim of the current study was to investigate the antiarthritic effect of gossypin against collagen-induced arthritis (CIA) in rats.
Methods: Intraperitoneal administration of Type II collagen (2 mg/mL) was used to induce arthritis in the rats, followed by oral administration of gossypin (5, 10 and 15 mg/kg) for 28 days.
Int J Cosmet Sci
January 2025
BioSpectrum Life Science Institute, A1805, U-TOWER, 767, Yongin, Republic of Korea.
When cellular ageing is accelerated by various extrinsic/endogenous stimuli, regenerative function deteriorates, and enriched secretomes, such as the senescence-associated secretory phenotype (SASP), contribute to chronic inflammation and cause matrix degeneration. SASPs from senescent fibroblasts exacerbate cellular senescence via autocrine signalling and also accelerate skin ageing through the induction of neighbouring cell senescence via paracrine signalling. The interaction between dermis fibroblasts and their neighbours, adipose-derived stem cells (ADSCs) in the hypodermis, which lies deep in the dermis, is a potential target for skin ageing.
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