scholarly journals Reply: Expanded Role for Bone Marrow–derived Hematopoietic Stem and Progenitor Cells in Pulmonary Arterial Hypertension

2016 ◽  
Vol 194 (3) ◽  
pp. 384-385
Author(s):  
Ling Yan ◽  
James West ◽  
Rizwan Hamid
Keyword(s):  
Bone Marrow ◽  
Pulmonary Arterial Hypertension ◽  
Arterial Hypertension ◽  
Progenitor Cells ◽  
Hematopoietic Stem ◽  
Stem And Progenitor Cells ◽  
Pulmonary Arterial

scholarly journals BMPR2‐expressing bone marrow‐derived endothelial‐like progenitor cells alleviate pulmonary arterial hypertension in vivo

Respirology ◽  
2019 ◽  
Vol 24 (11) ◽  
pp. 1095-1103 ◽  
Author(s):  
Rebecca L. Harper ◽  
Suzanne Maiolo ◽  
Rebekah J. Ward ◽  
Jemma Seyfang ◽  
Michaelia P. Cockshell ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Pulmonary Arterial Hypertension ◽  
Arterial Hypertension ◽  
Progenitor Cells ◽  
Pulmonary Arterial

scholarly journals Rescue of Monocrotaline-Induced Pulmonary Arterial Hypertension Using Bone Marrow–Derived Endothelial-Like Progenitor Cells

2005 ◽  
Vol 96 (4) ◽  
pp. 442-450 ◽  
Author(s):  
Yidan D. Zhao ◽  
David W. Courtman ◽  
Yupu Deng ◽  
Lakshmi Kugathasan ◽  
Qiuwang Zhang ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Pulmonary Arterial Hypertension ◽  
Arterial Hypertension ◽  
Progenitor Cells ◽  
Pulmonary Arterial

scholarly journals A Tm4sf1-Marked Subpopulation of Endothelial Stem/Progenitor Cells Identified by Lung Single-Cell Omics of Pulmonary Arterial Hypertension

2022 ◽  
Author(s):  
Jason Hong ◽  
Brenda Wong ◽  
Caroline Huynh ◽  
Brian Tang ◽  
Soban Umar ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Pulmonary Arterial Hypertension ◽  
Arterial Hypertension ◽  
Single Cell ◽  
Progenitor Cells ◽  
Cell Communication ◽  
Cell Phenotype ◽  
Hematopoietic Stem ◽  
Pulmonary Arterial ◽  
Lung Endothelial Cells

Rationale: The identification and role of endothelial progenitor cells (EPCs) in pulmonary arterial hypertension (PAH) remains controversial. Single-cell omics analysis can shed light on EPCs and their potential contribution to PAH pathobiology. Objectives: We aim to identify EPCs in rat lungs and assess their relevance to preclinical and human PAH. Methods: Differential expression, gene set enrichment, cell-cell communication, and trajectory reconstruction analyses were performed on lung endothelial cells from single-cell RNA-seq of Sugen-hypoxia, monocrotaline, and control rats. Relevance to human PAH was assessed in multiple independent blood and lung transcriptomic datasets. Measurements and Main Results: A subpopulation of endothelial cells (EA2) marked by Tm4sf1, a gene strongly implicated in cancer, harbored a distinct transcriptomic signature including Bmpr2 downregulation that was enriched for pathways such as inflammation and angiogenesis. Cell-to-cell communication networks specific to EA2 were activated in PAH such as CXCL12 signaling. Trajectory analysis demonstrated EA2 has a stem/progenitor cell phenotype. Analysis of independent datasets revealed Tm4sf1 is a marker for hematopoietic stem cells and is upregulated in PAH peripheral blood, particularly in patients with worse WHO functional class. EA2 signature genes including Procr and Sulf1 were found to be differentially regulated in the lungs of PAH patients and in PAH models in vitro, such as BMPR2 knockdown. Conclusions: Our study uncovered a novel Tm4sf1-marked stem/progenitor subpopulation of rat lung endothelial cells and demonstrated its relevance to preclinical and human PAH. Future experimental studies are warranted to further elucidate the pathogenic role and therapeutic potential of targeting EA2 and Tm4sf1 in PAH.

scholarly journals Bone Marrow-Derived Endothelial Progenitor Cells Contribute to Monocrotaline-Induced Pulmonary Arterial Hypertension in Rats via Inhibition of Store-Operated Ca2+ Channels

2018 ◽  
Vol 2018 ◽  
pp. 1-9 ◽  
Author(s):  
Ran Miao ◽  
Jun Wan ◽  
Jie Liu ◽  
Jason X.-J. Yuan ◽  
Jing Wang ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Pulmonary Arterial Hypertension ◽  
Arterial Hypertension ◽  
Right Ventricular ◽  
Progenitor Cells ◽  
Endothelial Progenitor Cells ◽  
Control Group ◽  
Trpc Channels ◽  
Endothelial Progenitor ◽  
Pulmonary Arterial

Purpose. This study aimed to explore whether bone marrow- (BM-) derived endothelial progenitor cells (EPCs) contributing to monocrotaline- (MCT-) induced pulmonary arterial hypertension (PAH) in rats via modulating store-operated Ca2+ channels (SOC). Methods. Sprague Dawley (SD) rats were assigned into MCT group (n = 30) and control group (n = 20). Rats in MCT group were subcutaneously administered with 60 mg/kg MCT solution, and rats in control group were injected with equal amount of vehicle. After 3 weeks of treatment, right ventricular systolic pressure (RVSP) and right ventricular hypertrophy index (RVHI) of two groups were measured, and BM-derived EPCs were isolated. Immunochemistry identification and vasculogenesis detection of EPCs were then performed. Ca2+cyt measurement was performed to detect store-operated calcium entry (SOCE) in two groups, followed by determination of Orai and canonical transient receptor potential (TRPC) channels expression. Results. After 3 weeks of treatment, there were significant increases in RVSP and RVHI in MCT group compared with control group, indicating that MCT successfully induced PAH in rats. Moreover, the SOCE (Ca2+cyt rise) in BM-derived EPCs of MCT group was lower than that of control group. Furthermore, the expression levels of Orai3, TRPC1, TRPC3, and TRPC6 in BM-derived EPCs were decreased in MCT group in comparison with control group. Conclusions. The SOC activities were inhibited in BM-derived EPCs of MCT-treated rats. These results may be associated with the depressed expression of Orai3, TRPC1, TRPC3, and TRPC6, which are major mediators of SOC.

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