Abstract
WISP1, as a member of the CCN4 protein family, has cell protective effects of promoting cell proliferation and inhibiting cell apoptosis. Although some studies have confirmed that WISP1 is concerned with colon cancer and lung cancer, there is little report about the influence of WISP1 in traumatic brain injury. Here, we found that the expression of WISP1 mRNA and protein decreased at 3 d and then increased at 5 d after traumatic brain injury (TBI). Meanwhile, immunofluorescence demonstrated that there was little colocation of WISP1 with GFAP, Iba1, and WISP1 colocalized with NeuN partly. WISP1 colocalized with LC3, but there was little of colocation about WISP1 with cleaved caspase-3. Subsequent study displayed that the expression of β-catenin protein was identical to that of WISP1 after TBI. WISP1 was mainly located in cytoplasm of PC12 or SHSY5Y cells. Compared with the negative control group, WISP1 expression reduced obviously in SHSY5Y cells transfected with WISP1 si-RNA. CCK-8 assay showed that pyrroloquinoline quinone (PQQ) had little influence on viability of PC12 and SHSY5Y cells. These results suggested that WISP1 played a protective role after traumatic brain injury in rats, and this effect might be relative to autophagy caused by traumatic brain injury.
Highlights
Traumatic brain injury (TBI), known as brain injury, is mainly caused by external mechanical forces
CCN protein family consists of 6 family members, including cysteine-rich protein 61 (CYR61/CNN1) and connective tissue growth factor (CTGF/CCN2), as well as nephroblastoma-overexpressed secreted protein (NOV/CCN3), WISP1 (CCN4), WISP2 (CCN5), and WISP3 (CCN6) [3]
The results showed that, compared with the sham group, WISP1 mRNA slightly decreased at 1 d, reached the minimum at 3 d after traumatic brain injury (TBI), and recovered at 5 d and 7 d after TBI
Summary
Traumatic brain injury (TBI), known as brain injury, is mainly caused by external mechanical forces. There were a series of pathological, physiological, and biochemical changes, such as subarachnoid hemorrhage, cerebral blood tube spasms, disturbance of cerebral circulation, and cerebral edema. All these secondary and primary brain injuries led to higher mortality rates. WISP1 (Wnt inducible signaling pathway protein 1) is a CCN family member, which is more broadly identified with development and tumorigenesis [2]. The CCN family is characterized by four cysteine-rich modular domains that include insulin-like growth factor-binding domain, von Willebrand factor type C module, thrombospondin domain, and C-terminal cysteine knot-like domain. WISP1 combinates leucine-rich proteoglycans and affects ability of the cell to anchor the extracellular matrix [4]
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
