title: Chlamydia pneumoniae infection promotes vascular endothelial cell angiogenesis through an IQGAP1-related signaling pathway.
abstract: Chlamydia pneumoniae (C. pneumoniae) infection plays a potential role in angiogenesis. However, it is still an enigma how C. pneumoniae is involved in this process. Therefore, we investigated the effect of C. pneumoniae infection on angiogenesis, and then explored the roles of IQGAP1-related signaling in C. pneumoniae infection-induced angiogenesis. C. pneumoniae infection significantly enhanced angiogenesis as assessed by the tube formation assay possibly by inducing vascular endothelial cell (VEC) migration in the wound healing and Transwell migration assays. Subsequently, immunoprecipitation, Western blot and tube formation assay results showed that the phosphorylation of both IQGAP1 and N-WASP was required for the angiogenesis induced by C. pneumoniae infection. Our co-immunoprecipitation study revealed that IQGAP1 physically associated with N-WASP after C. pneumoniae infection of VECs. Actin polymerization assay further showed that in C. pneumoniae-infected VECs, both IQGAP1 and N-WASP were recruited to filamentous actin, and shared some common compartments localized at the leading edge of lamellipodia, which was impaired after the depletion of IQGAP1 by using the small interference RNA. Moreover, the knockdown of IQGAP1 also significantly decreased N-WASP phosphorylation at Tyr256 induced by C. pneumoniae infection. We conclude that C. pneumoniae infection promotes VEC migration and angiogenesis presumably through the IQGAP1-related signaling pathway.
authors.affiliation: Department of Physiology and Pathophysiology, School of Basic Medical Sciences, Tianjin Medical University, No. 22 Qixiangtai Road, Heping District, Tianjin 300070, China.
authors.forename: Beibei
authors.initials: B
authors.lastname: Wang
authors.affiliation: Department of Physiology and Pathophysiology, School of Basic Medical Sciences, Tianjin Medical University, No. 22 Qixiangtai Road, Heping District, Tianjin 300070, China.
authors.forename: Lijun
authors.initials: L
authors.lastname: Zhang
authors.affiliation: Department of Physiology and Pathophysiology, School of Basic Medical Sciences, Tianjin Medical University, No. 22 Qixiangtai Road, Heping District, Tianjin 300070, China.
authors.forename: Jingya
authors.initials: J
authors.lastname: Liu
authors.affiliation: Department of Physiology and Pathophysiology, School of Basic Medical Sciences, Tianjin Medical University, No. 22 Qixiangtai Road, Heping District, Tianjin 300070, China.
authors.forename: Lu
authors.initials: L
authors.lastname: Ma
authors.affiliation: Department of Physiology and Pathophysiology, School of Basic Medical Sciences, Tianjin Medical University, No. 22 Qixiangtai Road, Heping District, Tianjin 300070, China.
authors.forename: Haiwei
authors.initials: H
authors.lastname: Wang
authors.affiliation: Department of Physiology and Pathophysiology, School of Basic Medical Sciences, Tianjin Medical University, No. 22 Qixiangtai Road, Heping District, Tianjin 300070, China.
authors.forename: Ningbo
authors.initials: N
authors.lastname: Zheng
authors.affiliation: Department of Physiology and Pathophysiology, School of Basic Medical Sciences, Tianjin Medical University, No. 22 Qixiangtai Road, Heping District, Tianjin 300070, China.
authors.forename: Xiaoyu
authors.initials: X
authors.lastname: Chen
authors.affiliation: Department of Physiology and Pathophysiology, School of Basic Medical Sciences, Tianjin Medical University, No. 22 Qixiangtai Road, Heping District, Tianjin 300070, China.
authors.forename: Bingling
authors.initials: B
authors.lastname: Shen
authors.affiliation: Department of Physiology and Pathophysiology, School of Basic Medical Sciences, Tianjin Medical University, No. 22 Qixiangtai Road, Heping District, Tianjin 300070, China.
authors.forename: Zhelong
authors.initials: Z
authors.lastname: Xu
authors.affiliation: Department of Physiology and Pathophysiology, School of Basic Medical Sciences, Tianjin Medical University, No. 22 Qixiangtai Road, Heping District, Tianjin 300070, China. Electronic address: lijunwz@hotmail.com.
authors.forename: Lijun
authors.initials: L
authors.lastname: Zhang
mesh_terms: D000199:Actins / Q000235:genetics / Q000378:metabolism; D002460:Cell Line; D002465:Cell Movement; D023521:Chlamydophila Infections / Q000150:complications / Q000382:microbiology; D016993:Chlamydophila pneumoniae; D042783:Endothelial Cells / Q000166:cytology* / Q000382:microbiology; D006801:Humans; D009389:Neovascularization, Pathologic / Q000382:microbiology*; D010766:Phosphorylation; D011493:Protein Kinase C / Q000378:metabolism; D034741:RNA, Small Interfering / Q000235:genetics; D015398:Signal Transduction; D051317:Wiskott-Aldrich Syndrome Protein, Neuronal / Q000378:metabolism; D020703:ras GTPase-Activating Proteins / Q000378:metabolism*; D019061:src-Family Kinases / Q000378:metabolism
chemical_list: D000199:Actins; C101203:IQ motif containing GTPase activating protein 1; D034741:RNA, Small Interfering; C495771:WASL protein, human; D051317:Wiskott-Aldrich Syndrome Protein, Neuronal; D020703:ras GTPase-Activating Proteins; D019061:src-Family Kinases; D011493:Protein Kinase C
keywords: Angiogenesis; Chlamydia pneumoniae; IQ domain GTPase-activating protein 1; Neural Wiskott-Aldrich syndrome protein; Vascular endothelial cell