Abstract
Objective: Hypertensive intracerebral hemorrhage (ICH) has a high mortality rate, but there is no effective treatment,so how to prevent it has become a top priority. Heat shock protein 47 (HSP47) is a molecular chaperone for collagen synthesis and is responsible for transporting procollagen from the endoplasmic reticulum to the golgi lumen, effectively maintaining the three-dimensional structure of collagen. Absence of HSP47 may affect collagen synthesis and the stability of extracellular matrix (ECM), further damaging the stability of blood vessels. Therefore, we aimed to explore the role of HSP47 in ICH. Design and method: Spontaneous hypertensive ICH of mice were induced by angiotensin II and L-NAME We found that the level of HSP47 gradually decreased with the increase of modelling days. The adeno-associated virus was delivered into brain by stereotactic injection to overexpress HSP47. Results: The incidence of ICH were decreased significantly in mice by HSP47 overexpression. At the same time, the number and size of ICH in mice were significantly reduced. Experimental results show that HSP47 overexpression was sufficient to enhance ECM integrity and reduce VSMC apoptosis before ICH. Conclusions: These results suggest that HSP47 may have a protective effect on hypertensive ICH. Therefore, we emphasize that overexpression of HSP47 may be a new strategy for clinical treatment of hypertensive ICH.
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