| First Author | Poirier C | Year | 2011 |
| Journal | Respir Physiol Neurobiol | Volume | 179 |
| Issue | 2-3 | Pages | 334-7 |
| PubMed ID | 21907835 | Mgi Jnum | J:215226 |
| Mgi Id | MGI:5604907 | Doi | 10.1016/j.resp.2011.08.012 |
| Citation | Poirier C, et al. (2011) TIMAP protects endothelial barrier from LPS-induced vascular leakage and is down-regulated by LPS. Respir Physiol Neurobiol 179(2-3):334-7 |
| abstractText | TIMAP is a regulatory subunit of protein phosphatase 1, whose role remains largely unknown. Our recent data suggested that TIMAP is involved in the regulation of barrier function in cultured pulmonary endothelial monolayers [Csortos et al., 2008. Am. J. Physiol. Lung Cell. Mol. Physiol. 295, L440-L450]. Here we showed that TIMAP depletion exacerbates lipopolysaccharide (LPS)-induced vascular leakage in murine lung, suggesting that TIMAP has a barrier-protective role in vivo. Real-Time RT PCR analysis revealed that treatment with LPS significantly suppressed Timap mRNA level. This suppression was not achieved via the down-regulation of Timap promoter activity, suggesting that LPS decreased Timap mRNA stability. Pretreatment with protein kinase A (PKA) inhibitor H-89 reduced TIMAP mRNA level, whereas pretreatment with PKA activator, bnz-cAMP, increased this level and attenuated LPS-induced decrease in TIMAP mRNA. Altogether, these data confirmed the barrier-protective role of TIMAP and suggested that barrier-disruptive and barrier-protective agents may employ modulation of TIMAP expression as a mechanism affecting barrier permeability. |
