Periostin‐related progression of different types of experimental pulmonary hypertension: A role for M2 macrophage and FGF‐2 signalling

Abstract

Background and objective: Remodelling of pulmonary arteries (PA) contributes to the progression of pulmonary hypertension (PH). Periostin, a matricellular protein, has been reported to be involved in the development of PH. We examined the role of periostin in the pathogenesis of PH using different types of experimental PH. Methods: PH was induced by vascular endothelial growth factor receptor antagonist (Sugen5416) plus hypoxic exposure (SuHx) and venous injection of monocrotalinepyrrole (MCT-P) in wild-type (WT) and periostin À/À mice. Pulmonary haemodynamics, PA remodelling, expression of chemokines and fibroblast growth factor (FGF)-2, accumulation of macrophages to small PA and the right ventricle (RV) were examined in PHinduced WT and periostin À/À mice. Additionally, the role of periostin in the migration of macrophages, human PA smooth muscle (HPASMCs) and endothelial cells (HPMVECs) was investigated. Results: In PH induced by SuHx and MCT-P, PH and accumulation of M2 macrophage to small PA were attenuated in periostin À/À mice. PA remodelling post-SuHx treatment was also mild in periostin À/À mice compared to WT mice. Expression of macrophage-associated chemokines and FGF-2 in lung tissue, and accumulation of CD68-positive cells in the RV were less in SuHx periostin À/À than in SuHx WT mice. Periostin secretion in HPASMCs and HPMVECs was enhanced by transforming growth factor-β. Periostin also augmented macrophage, HPASMCs and HPMVECs migration. Separately, serum periostin levels were significantly elevated in patients with PH compared to healthy controls. Conclusion: Periostin is involved in the development of different types of experimental PH, and may also contribute to the pathogenesis of human PH.

Preliminary Mechanism of Glial Maturation Factor β on Pulmonary Vascular Remodeling in Pulmonary Arterial Hypertension

“…It can be induced by TGFβ1, 2 and 3, BMP2 and 4, VEGFA, CTGF, vitamin K and IL‐3, 4, 6 and 13 [ 6,8,9 ] and other inflammation cytokines. [ 39–41 ] POSTN could augment macrophage, HPASMCs, and HPMVECs migration; knockout POSTN attenuated the pulmonary arteries (PA) remodeling and accumulation of M2 macrophage to small PA. [ 42 ] In the present study, we also found that increased POSTN expression was accompanied by the upregulation of inflammatory factors; in contrast, knockout GMFβ reduced POSTN expression as well as the expression of inflammatory factors. Therefore, we supposed GMFβ may mediate POSTN through some inflammatory factors or some inflammatory pathways.…”

The Identification of Key Genes and Biological Pathways in Polycystic Ovary Syndrome and its Complications by Next Generation Squancing (NGS) and Bioinformatics Analysis

“…CASP1 [185], FOXP3 [186], SOCS1 [187], GATA6 [188], IRF7 [189], POSTN (periostin) [190], CYP19A1 [191], CD36 [192], LYN (LYN proto-oncogene, Src family tyrosine kinase) [193], CD4 [194], LEPR (leptin receptor) [195], AR (androgen receptor) [196], FOXO1 [197] and PON2 [198] are a potential biomarkers for the detection and prognosis of PCOS. Udjus et al [199] Benjafield et al [200], Shetty et al [58], Kassan et al [201], Wetzl et al [202], Le Hiress et al [203], Pal-Ghosh et al [204], Niu, [205], Fan et al [206], Deng et al [207], Chen et al [208], Sardo et al [209], Seidel et al [210], Zhu et al [211], Omura et al [212], Hu et al [213], Castoldi et al [214], Yoshida et al [215], Palao et al [216], Kušíková et al [217], Decharatchakul et al [218], Ahmed et al [219], Merklinger et al [220], Lei et al [146], Liu et al [221], Chen et al [222], Tan et al [223], Shi et al [224], Ikonnikova et al [225], Shimodaira et al [226], Pravenec et al [227], Zhang et al [228], Shah et al [229], Cicekliyurt and Dermenci [230], Ong et al [98], Nowzari et al [163], Kim et al [231], Bonafiglia et al [232], Selle et al [233],Yoo et al [234], Kasacka et al [235], Wang et al [236], Huang et al [237], Caceres et al [238], Lei et al [239], Lu et al [240], Cui et al [241], Xiao et al [242], Hiramatsu et al [243], Oliver et al [244], Grabowski et al [245], Zhu et al [246] and Li et al [247] demonstrated that the altered expression of CASP1, EDNRA (endothelin receptor type A), F2RL1, FOXP3, TIMP4, CD74, PLK1, TGFB1, GATA6, IRF7, IRF9, BGN (biglycan), C...…”

Study on potential differentially expressed genes in idiopathic pulmonary fibrosis by bioinformatics and next generation sequencing data analysis

“…CX3CR1 [395], S100A12 [396], MPO (myeloperoxidase) [397], RXFP1 [398], S100A8 [399], CXCL11 [373], CBS (cystathionine beta-synthase) [400], WNT7A [401], BDNF (brain derived neurotrophic factor) [402], CXCL10 [403], CCL8 [404], FCGR3B [405], S100A9 [406], IL1B [407], CXCR2 [408], WNT3A [409], BMI1 [410], STC1 [411], ABCA3 [412], CD36 [413], TRIB3 [414], GPX3 [415], FGF2 [416], FASN (fatty acid synthase) [417], SHH (sonic hedgehog signaling molecule) [418], DACH1 [419], FGF9 [420], SLC7A11 [421], VIP (vasoactive intestinal peptide) [422], KL (klotho) [423], BMPR2 [424], APOA1 [425], LRRK2 [426], TLR3 [427], GATA3 [428], RSPO2 [429], CCR2 [430], NEK7 [431], BMPER (BMP binding endothelial regulator) [432], CAV1 [433], CR1 [434], TFPI (tissue factor pathway inhibitor) [435], AP1S2 [436], FOXJ1 [437], AQP5 [438], MUC16 [439] and MUC4 [440] could be used as a therapeutic target for IPF. CX3CR1 [441], S100A12 [442], PF4 [443], MPO (myeloperoxidase) [444], WNT7A [445], SLC6A4 [446], BDNF (brain derived neurotrophic factor) [447], CXCL10 [448], NEK7 [449], CYP1B1 [450], ABCA3 [451], TRIB3 [452], PCSK9 [453], FGF2 [454], ACKR4 [455], FASN (fatty acid synthase) [456], VIP (vasoactive intestinal peptide) [457], KL (klotho) [458], BMPR2 [459], APOA1 [323], TLR3 [460], CCR2 [461], TLR7 [462], CAV1 [463], WWC2 [464], TFPI (tissue factor pathway inhib...…”