Cyclosporine A stimulated hair growth from mouse vibrissae follicles in an organ culture model

Hypertrichosis is one of the most common side effects of systemic cyclosporine A therapy.It has been previously shown that cyclosporine A induces anagen and inhibits catagen development in mice.In the present study,to explore the mechanisms of cyclosporine A,we investigated the effects of cyclosporine A on hair shaft elongation,hair follicle cell proliferation,apoptosis,and mRNA expression of selected growth factors using an organ culture model of mouse vibrissae.In this model,cyclosporine A stimulated hair growth of normal mouse vibrissae follicles by inhibiting catagen-like development and promoting matrix cell proliferation.In addition,cyclosporine A caused an increase in the expression of vascular endothelial growth factor（VEGF）,hepatocyte growth factor（HGF）,and nerve growth factor（NGF）,and inhibited follistatin expression.Our findings provide an explanation for the clinically observed effects of cyclosporine A on hair growth.The mouse vibrissae organ culture offers an attractive model for identifying factors involved in the modulation of hair growth.

Emerging role of protein modification in inflammatory bowel disease

The onset of inflammatory bowel disease(IBD)involves many factors,including environmental parameters,microorganisms,and the immune system.Although research on IBD continues to expand,the specific pathogenesis mechanism is still unclear.Protein modification refers to chemical modification after protein biosynthesis,also known as post-translational modification(PTM),which causes changes in the properties and functions of proteins.Since proteins can be modified in different ways,such as acetylation,methylation,and phosphorylation,the functions of proteins in different modified states will also be different.Transitions between different states of protein or changes in modification sites can regulate protein properties and functions.Such modifications like neddylation,sumoylation,glycosylation,and acetylation can activate or inhibit various signaling pathways(e.g.,nuclear factor-κB(NF-κB),extracellular signal-regulated kinase(ERK),and protein kinase B(AKT))by changing the intestinal flora,regulating immune cells,modulating the release of cytokines such as interleukin-1β(IL-1β),tumor necrosis factor-α(TNF-α),and interferon-γ(IFN-γ),and ultimately leading to the maintenance of the stability of the intestinal epithelial barrier.In this review,we focus on the current understanding of PTM and describe its regulatory role in the pathogenesis of IBD.