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Comparative Proteomic Profiling of Exosomes Derived from Sema6A-Knockdown hPMVECs

ABSTRACT: This project aims to characterize the proteomic landscape of extracellular vesicles (EVs) released by human pulmonary microvascular endothelial cells (hPMVECs) following Sema6A gene knockdown. Using lentiviral-mediated RNA interference, we generated stable Sema6A-knockdown cell lines (*sh-Sema6A*) alongside negative control cells (sh-NC). Exosomes were isolated from conditioned media of both groups via ultracentrifugation and validated for EV-specific markers (e.g., CD63, TSG101). Subsequent high-resolution tandem mass spectrometry (LC-MS/MS)-based proteomic analysis will quantitatively compare protein cargoes between *sh-Sema6A*-EVs and sh-NC-EVs. This study seeks to identify Sema6A-regulated exosomal proteins implicated in endothelial cell communication, angiogenesis, or vascular pathophysiology, providing mechanistic insights into semaphorin signaling pathways in the pulmonary vasculature.

ORGANISM(S): Homo Sapiens

SUBMITTER: Tian Jiang

PROVIDER: PXD066691 | iProX | Mon Jul 28 00:00:00 BST 2025

REPOSITORIES: iProX

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Project description:Human herpesvirus-8 (HHV-8) is the causative agent of Kaposiâs sarcoma and is associated with the angioproliferative disorders primary effusion lymphoma (PEL) and multicentric Castlemanâs disease (MCD). We have previously described evidence of HHV-8 infection within the pulmonary vasculature of patients with idiopathic pulmonary arterial hypertension (IPAH). We speculated that viral infection of the pulmonary microvascular endothelial cells could cause the angioproliferative phenotype characteristic of severe pulmonary arterial hypertension (PAH). We now demonstrate the ability of HHV-8 to infect human pulmonary microvascular endothelial cells (HPMVECs) in vitro, confirming both latent and lytic infection. HHV-8 infection of HPMVECs resulted in significant changes of gene expression including alterations of pathways integral to both cellular apoptosis and angiogenesis. This infection also results in alterations of genes integral to the bone morphogenic protein (BMP) pathway, including down regulation of bone morphogenic protein receptor 1a (BMPR1a) and bone morphogenic protein 4 (BMP4). Other genes previously implicated in the development of PAH are also altered in expression by HHV-8 infection. These include increased expression of Interleukin-6 (IL-6) and the matrix metalloproteinases (MMP)-1, MMP-2 and MMP-10. Lastly, cells infected with HHV-8 apoptosis resistant. Infection of pulmonary microvascular endothelial cells with human herepesvirus-8 results in alteration of the BMP pathway as well as an anti-apoptotic phenotype, consistent with the development of plexiform lesions characteristic of pulmonary arterial hypertension. Experiment Overall Design: â¢ Direct comparison of HHV8-infected and mock-infected human pulmonary microvascular endothelial cells. Experiment Overall Design: â¢ Triplicate infection and mock infection samples were prepared. One hybridization per sample, 6 total hybridizations Experiment Overall Design: â¢ Single channel hybridization (no reference).

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Comparative Proteomic Profiling of Exosomes Derived from Sema6A-Knockdown hPMVECs

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