| First Author | Nidegawa-Saitoh Y | Year | 2018 |
| Journal | Cell Tissue Res | Volume | 374 |
| Issue | 2 | Pages | 329-338 |
| PubMed ID | 29971480 | Mgi Jnum | J:277543 |
| Mgi Id | MGI:6296184 | Doi | 10.1007/s00441-018-2878-y |
| Citation | Nidegawa-Saitoh Y, et al. (2018) Impaired healing of cornea incision injury in a TRPV1-deficient mouse. Cell Tissue Res 374(2):329-338 |
| abstractText | The present study attempts to elucidate the role of TRPV1 cation channel receptor on primary repair in an incision-wounded mouse cornea in vivo. Previous study revealed that blocking TRPV1 suppressed myofibroblast formation and expression of transforming growth factor beta1 (TGFbeta1) in cultured keratocytes or ocular fibroblasts. Male C57BL/6 (wild-type; WT) mice and male C57BL/6 Trpv1-null (KO) mice incurred a full-thickness incision injury (1.8 mm in length, limbus to limbus) in the central cornea of one eye with a surgical blade under general and topical anesthesia. The injury was not sutured. On days 0, 5, and 10, the eyes were enucleated, processed for histology, immunohistochemistry, and real-time RT-PCR gene expression analysis to evaluate the effects of the loss of TRPV1 on primary healing. Electron microscopy observation was also performed to know the effect of the loss of TRPV1 on ultrastructure of keratocytes. The results showed that the loss of Trpv1 gene delayed closure of corneal stromal incision with hindered myofibroblast transdifferentiation along with declines in the expression of collagen Ia1 and TGFbeta1. Inflammatory cell infiltration was not affected by the loss of TRPV1. Ultrastructurally endoplasmic reticulum of TRPV1-null keratocytes was more extensively dilated as compared with WT keratocytes, suggesting an impairment of protein secretion by TRPV1-gene knockout. These results indicate that injury-related TRPV1 signal is involved in healing of stromal incision injury in a mouse cornea by selectively stimulating TGFbeta-induced granulation tissue formation. |
