The effect of CRISPLD2 on TGFß-induced fibroblast fibrosis

Systemic sclerosis (SSc) is an autoimmune connective tissue disease involving multiple organs. The most common clinical symptom of SSc is progressive fibrosis of the skin, and the pathologically manifestations of skin were activation and proliferation of fibroblasts and continuous proliferation of extracellular matrix. Transforming growth factor ß (TGFß) can promote the proliferation and activation of fibroblasts, causing excessive deposition of collagen and structural proteins, and thereby causing fibrosis and dysfunction of tissues and organs. In this study, human cysteine-rich secreted protein LCCL domain protein 2 (CRISPLD2) was found increased reactivity in TGFß induced fibroblasts, and we further confirmed that CRISPLD2 can participate in TGFß induced fibroblast fibrosis from multiple perspectives and levels, and investigated the mechanism of CRISPLD2 in fibrosis, providing evidence for CRISPLD2 to become a clinical potential therapeutic target and a new biomarker. Overall design: We examined the effect of CRISPLD2 on fibrosis genes by knocking down the expression of CRISPLD2 or up-regulating CRISPLD2 expression in human fibroblasts.