International journal of molecular medicine
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Coronary artery disease (CAD) or atherosclerotic heart disease is one of the most common types of cardiovascular disease. Although percutaneous coronary intervention [PCI or percutaneous transluminal coronary angioplasty (PTCA)] is a mature, well-established technique used to treat atherosclerotic heart disease, its long‑term therapeutic effects are compromised by a high incidence of vascular restenosis (RS) following angioplasty. In our previous study, we found that the principal gap junction protein, connexin 43 (Cx43), in vascular smooth muscle cells (VSMCs) was involved in the development of vascular RS following angioplasty-induced balloon injury. ⋯ Notably, the knockdown of Cx43 also effectively attenuated the development of vascular RS and intimal hyperplasia following balloon injury in vivo. Taken together, our data suggest that Cx43 is involved in the development of vascular RS and intimal hyperplasia through the regulation of the proliferation and migration of VSMCs. Thus, the present study provides new insight into the pathogenesis of vascular RS, and suggests that further comfirms that Cx43 may well be a novel potential pharmacological target for preventing vascular RS following PCI.
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The function of microRNAs (miRNAs or miRs) in regulating neuropathic pain has attracted increasing attention in recent years. However, the precise mechanism of miRNAs in neuropathic pain remains largely unknown. In the present study, an important role of miR‑141 and its putative target gene, high‑mobility group box‑1 (HMGB1), was demonstrated in a rat model of neuropathic pain induced by chronic constriction injury (CCI). ⋯ Overexpression of miR‑141 significantly suppressed the expression of HMGB1 in vitro and in vivo. Furthermore, overexpression of HMGB1 apparently abrogated the beneficial effect of miR‑141 on inhibiting neuropathic pain. Taken together, the data suggest that overexpression of miR‑141 alleviates neuropathic pain development via targeting and inhibiting HMGB1, implying that blocking HMGB1 by miR‑141 could be a useful therapeutic strategy for the treatment of neuropathic pain.