Molecular mechanisms regulating wound repair: Evidence for paracrine signaling from corneal epithelial cells to fibroblasts and immune cells following transient epithelial cell tre...

Autores: Pal Ghosh, Sonali; Karpinski, Beverly A.; Datta Majumdar, Himani; Ghosh, Trisha; Thomasian, Julie; Brooks, Stephen R.; Sawaya, Andrew P.; Morasso, Maria I.; Scholand, Kaitlin K.; de Paiva, Cintia S.; Galletti, Jeremías Gastón; Stepp, Mary Ann
Año de publicación: 2023
Idioma: inglés
Tipo de recurso: artículo
Estado: versión publicada
Descripción: In this paper, we use RNAseq to identify senescence and phagocytosis as key factors to understanding how mitomyin C (MMC) stimulates regenerative wound repair. We use conditioned media (CM) from untreated (CMC) and MMC treated (CMM) human and mouse corneal epithelial cells to show that corneal epithelial cells indirectly exposed to MMC secrete elevated levels of immunomodulatory proteins including IL-1α and TGFβ1 compared to cells exposed to CMC. These factors increase epithelial and macrophage phagocytosis and promote ECM turnover. IL-1α supplementation can increase phagocytosis in control epithelial cells and attenuate TGFβ1 induced αSMA expression by corneal fibroblasts. Yet, we show that epithelial cell CM contains factors besides IL-1α that regulate phagocytosis and αSMA expression by fibroblasts. Exposure to CMM also impacts the activation of bone marrow derived dendritic cells and their ability to present antigen. These in vitro studies show how a brief exposure to MMC induces corneal epithelial cells to release proteins and other factors that function in a paracrine way to enhance debris removal and enlist resident epithelial and immune cells as well as stromal fibroblasts to support regenerative and not fibrotic wound healing.
Fil: Pal Ghosh, Sonali. The George Washington University; Estados Unidos
Fil: Karpinski, Beverly A.. The George Washington University; Estados Unidos
Fil: Datta Majumdar, Himani. The George Washington University; Estados Unidos
Fil: Ghosh, Trisha. The George Washington University; Estados Unidos
Fil: Thomasian, Julie. The George Washington University; Estados Unidos
Fil: Brooks, Stephen R.. National Institutes of Health; Estados Unidos
Fil: Sawaya, Andrew P.. National Institutes of Health; Estados Unidos
Fil: Morasso, Maria I.. National Institutes of Health; Estados Unidos
Fil: Scholand, Kaitlin K.. Baylor College of Medicine; Estados Unidos
Fil: de Paiva, Cintia S.. Baylor College of Medicine; Estados Unidos
Fil: Galletti, Jeremías Gastón. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Medicina Experimental. Academia Nacional de Medicina de Buenos Aires. Instituto de Medicina Experimental; Argentina
Fil: Stepp, Mary Ann. The George Washington University; Estados Unidos
Materia: cornea
mitomycin C
wound healing
corneal epithelial cell
Nivel de accesibilidad: acceso abierto
Condiciones de uso: https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
Repositorio
Institución: Consejo Nacional de Investigaciones Científicas y Técnicas
OAI Identificador: oai:ri.conicet.gov.ar:11336/227661

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repository_id_str	3498
network_name_str	CONICET Digital (CONICET)
spelling	Molecular mechanisms regulating wound repair: Evidence for paracrine signaling from corneal epithelial cells to fibroblasts and immune cells following transient epithelial cell treatment with Mitomycin CPal Ghosh, SonaliKarpinski, Beverly A.Datta Majumdar, HimaniGhosh, TrishaThomasian, JulieBrooks, Stephen R.Sawaya, Andrew P.Morasso, Maria I.Scholand, Kaitlin K.de Paiva, Cintia S.Galletti, Jeremías GastónStepp, Mary Anncorneamitomycin Cwound healingcorneal epithelial cellhttps://purl.org/becyt/ford/3.2https://purl.org/becyt/ford/3In this paper, we use RNAseq to identify senescence and phagocytosis as key factors to understanding how mitomyin C (MMC) stimulates regenerative wound repair. We use conditioned media (CM) from untreated (CMC) and MMC treated (CMM) human and mouse corneal epithelial cells to show that corneal epithelial cells indirectly exposed to MMC secrete elevated levels of immunomodulatory proteins including IL-1α and TGFβ1 compared to cells exposed to CMC. These factors increase epithelial and macrophage phagocytosis and promote ECM turnover. IL-1α supplementation can increase phagocytosis in control epithelial cells and attenuate TGFβ1 induced αSMA expression by corneal fibroblasts. Yet, we show that epithelial cell CM contains factors besides IL-1α that regulate phagocytosis and αSMA expression by fibroblasts. Exposure to CMM also impacts the activation of bone marrow derived dendritic cells and their ability to present antigen. These in vitro studies show how a brief exposure to MMC induces corneal epithelial cells to release proteins and other factors that function in a paracrine way to enhance debris removal and enlist resident epithelial and immune cells as well as stromal fibroblasts to support regenerative and not fibrotic wound healing.Fil: Pal Ghosh, Sonali. The George Washington University; Estados UnidosFil: Karpinski, Beverly A.. The George Washington University; Estados UnidosFil: Datta Majumdar, Himani. The George Washington University; Estados UnidosFil: Ghosh, Trisha. The George Washington University; Estados UnidosFil: Thomasian, Julie. The George Washington University; Estados UnidosFil: Brooks, Stephen R.. National Institutes of Health; Estados UnidosFil: Sawaya, Andrew P.. National Institutes of Health; Estados UnidosFil: Morasso, Maria I.. National Institutes of Health; Estados UnidosFil: Scholand, Kaitlin K.. Baylor College of Medicine; Estados UnidosFil: de Paiva, Cintia S.. Baylor College of Medicine; Estados UnidosFil: Galletti, Jeremías Gastón. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Medicina Experimental. Academia Nacional de Medicina de Buenos Aires. Instituto de Medicina Experimental; ArgentinaFil: Stepp, Mary Ann. The George Washington University; Estados UnidosAcademic Press Ltd - Elsevier Science Ltd2023-02info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionhttp://purl.org/coar/resource_type/c_6501info:ar-repo/semantics/articuloapplication/pdfapplication/pdfapplication/pdfhttp://hdl.handle.net/11336/227661Pal Ghosh, Sonali; Karpinski, Beverly A.; Datta Majumdar, Himani; Ghosh, Trisha; Thomasian, Julie; et al.; Molecular mechanisms regulating wound repair: Evidence for paracrine signaling from corneal epithelial cells to fibroblasts and immune cells following transient epithelial cell treatment with Mitomycin C; Academic Press Ltd - Elsevier Science Ltd; Experimental Eye Research; 227; 109353; 2-2023; 1-180014-4835CONICET DigitalCONICETenginfo:eu-repo/semantics/altIdentifier/doi/10.1016/j.exer.2022.109353info:eu-repo/semantics/altIdentifier/url/https://www.sciencedirect.com/science/article/pii/S0014483522004341info:eu-repo/semantics/openAccesshttps://creativecommons.org/licenses/by-nc-sa/2.5/ar/reponame:CONICET Digital (CONICET)instname:Consejo Nacional de Investigaciones Científicas y Técnicas2025-09-29T10:23:03Zoai:ri.conicet.gov.ar:11336/227661instacron:CONICETInstitucionalhttp://ri.conicet.gov.ar/Organismo científico-tecnológicoNo correspondehttp://ri.conicet.gov.ar/oai/requestdasensio@conicet.gov.ar; lcarlino@conicet.gov.arArgentinaNo correspondeNo correspondeNo correspondeopendoar:34982025-09-29 10:23:03.857CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicasfalse
dc.title.none.fl_str_mv	Molecular mechanisms regulating wound repair: Evidence for paracrine signaling from corneal epithelial cells to fibroblasts and immune cells following transient epithelial cell treatment with Mitomycin C
title	Molecular mechanisms regulating wound repair: Evidence for paracrine signaling from corneal epithelial cells to fibroblasts and immune cells following transient epithelial cell treatment with Mitomycin C
spellingShingle	Molecular mechanisms regulating wound repair: Evidence for paracrine signaling from corneal epithelial cells to fibroblasts and immune cells following transient epithelial cell treatment with Mitomycin C Pal Ghosh, Sonali cornea mitomycin C wound healing corneal epithelial cell
title_short	Molecular mechanisms regulating wound repair: Evidence for paracrine signaling from corneal epithelial cells to fibroblasts and immune cells following transient epithelial cell treatment with Mitomycin C
title_full	Molecular mechanisms regulating wound repair: Evidence for paracrine signaling from corneal epithelial cells to fibroblasts and immune cells following transient epithelial cell treatment with Mitomycin C
title_fullStr	Molecular mechanisms regulating wound repair: Evidence for paracrine signaling from corneal epithelial cells to fibroblasts and immune cells following transient epithelial cell treatment with Mitomycin C
title_full_unstemmed	Molecular mechanisms regulating wound repair: Evidence for paracrine signaling from corneal epithelial cells to fibroblasts and immune cells following transient epithelial cell treatment with Mitomycin C
title_sort	Molecular mechanisms regulating wound repair: Evidence for paracrine signaling from corneal epithelial cells to fibroblasts and immune cells following transient epithelial cell treatment with Mitomycin C
dc.creator.none.fl_str_mv	Pal Ghosh, Sonali Karpinski, Beverly A. Datta Majumdar, Himani Ghosh, Trisha Thomasian, Julie Brooks, Stephen R. Sawaya, Andrew P. Morasso, Maria I. Scholand, Kaitlin K. de Paiva, Cintia S. Galletti, Jeremías Gastón Stepp, Mary Ann
author	Pal Ghosh, Sonali
author_facet	Pal Ghosh, Sonali Karpinski, Beverly A. Datta Majumdar, Himani Ghosh, Trisha Thomasian, Julie Brooks, Stephen R. Sawaya, Andrew P. Morasso, Maria I. Scholand, Kaitlin K. de Paiva, Cintia S. Galletti, Jeremías Gastón Stepp, Mary Ann
author_role	author
author2	Karpinski, Beverly A. Datta Majumdar, Himani Ghosh, Trisha Thomasian, Julie Brooks, Stephen R. Sawaya, Andrew P. Morasso, Maria I. Scholand, Kaitlin K. de Paiva, Cintia S. Galletti, Jeremías Gastón Stepp, Mary Ann
author2_role	author author author author author author author author author author author
dc.subject.none.fl_str_mv	cornea mitomycin C wound healing corneal epithelial cell
topic	cornea mitomycin C wound healing corneal epithelial cell
purl_subject.fl_str_mv	https://purl.org/becyt/ford/3.2 https://purl.org/becyt/ford/3
dc.description.none.fl_txt_mv	In this paper, we use RNAseq to identify senescence and phagocytosis as key factors to understanding how mitomyin C (MMC) stimulates regenerative wound repair. We use conditioned media (CM) from untreated (CMC) and MMC treated (CMM) human and mouse corneal epithelial cells to show that corneal epithelial cells indirectly exposed to MMC secrete elevated levels of immunomodulatory proteins including IL-1α and TGFβ1 compared to cells exposed to CMC. These factors increase epithelial and macrophage phagocytosis and promote ECM turnover. IL-1α supplementation can increase phagocytosis in control epithelial cells and attenuate TGFβ1 induced αSMA expression by corneal fibroblasts. Yet, we show that epithelial cell CM contains factors besides IL-1α that regulate phagocytosis and αSMA expression by fibroblasts. Exposure to CMM also impacts the activation of bone marrow derived dendritic cells and their ability to present antigen. These in vitro studies show how a brief exposure to MMC induces corneal epithelial cells to release proteins and other factors that function in a paracrine way to enhance debris removal and enlist resident epithelial and immune cells as well as stromal fibroblasts to support regenerative and not fibrotic wound healing. Fil: Pal Ghosh, Sonali. The George Washington University; Estados Unidos Fil: Karpinski, Beverly A.. The George Washington University; Estados Unidos Fil: Datta Majumdar, Himani. The George Washington University; Estados Unidos Fil: Ghosh, Trisha. The George Washington University; Estados Unidos Fil: Thomasian, Julie. The George Washington University; Estados Unidos Fil: Brooks, Stephen R.. National Institutes of Health; Estados Unidos Fil: Sawaya, Andrew P.. National Institutes of Health; Estados Unidos Fil: Morasso, Maria I.. National Institutes of Health; Estados Unidos Fil: Scholand, Kaitlin K.. Baylor College of Medicine; Estados Unidos Fil: de Paiva, Cintia S.. Baylor College of Medicine; Estados Unidos Fil: Galletti, Jeremías Gastón. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Medicina Experimental. Academia Nacional de Medicina de Buenos Aires. Instituto de Medicina Experimental; Argentina Fil: Stepp, Mary Ann. The George Washington University; Estados Unidos
description	In this paper, we use RNAseq to identify senescence and phagocytosis as key factors to understanding how mitomyin C (MMC) stimulates regenerative wound repair. We use conditioned media (CM) from untreated (CMC) and MMC treated (CMM) human and mouse corneal epithelial cells to show that corneal epithelial cells indirectly exposed to MMC secrete elevated levels of immunomodulatory proteins including IL-1α and TGFβ1 compared to cells exposed to CMC. These factors increase epithelial and macrophage phagocytosis and promote ECM turnover. IL-1α supplementation can increase phagocytosis in control epithelial cells and attenuate TGFβ1 induced αSMA expression by corneal fibroblasts. Yet, we show that epithelial cell CM contains factors besides IL-1α that regulate phagocytosis and αSMA expression by fibroblasts. Exposure to CMM also impacts the activation of bone marrow derived dendritic cells and their ability to present antigen. These in vitro studies show how a brief exposure to MMC induces corneal epithelial cells to release proteins and other factors that function in a paracrine way to enhance debris removal and enlist resident epithelial and immune cells as well as stromal fibroblasts to support regenerative and not fibrotic wound healing.
publishDate	2023
dc.date.none.fl_str_mv	2023-02
dc.type.none.fl_str_mv	info:eu-repo/semantics/article info:eu-repo/semantics/publishedVersion http://purl.org/coar/resource_type/c_6501 info:ar-repo/semantics/articulo
format	article
status_str	publishedVersion
dc.identifier.none.fl_str_mv	http://hdl.handle.net/11336/227661 Pal Ghosh, Sonali; Karpinski, Beverly A.; Datta Majumdar, Himani; Ghosh, Trisha; Thomasian, Julie; et al.; Molecular mechanisms regulating wound repair: Evidence for paracrine signaling from corneal epithelial cells to fibroblasts and immune cells following transient epithelial cell treatment with Mitomycin C; Academic Press Ltd - Elsevier Science Ltd; Experimental Eye Research; 227; 109353; 2-2023; 1-18 0014-4835 CONICET Digital CONICET
url	http://hdl.handle.net/11336/227661
identifier_str_mv	Pal Ghosh, Sonali; Karpinski, Beverly A.; Datta Majumdar, Himani; Ghosh, Trisha; Thomasian, Julie; et al.; Molecular mechanisms regulating wound repair: Evidence for paracrine signaling from corneal epithelial cells to fibroblasts and immune cells following transient epithelial cell treatment with Mitomycin C; Academic Press Ltd - Elsevier Science Ltd; Experimental Eye Research; 227; 109353; 2-2023; 1-18 0014-4835 CONICET Digital CONICET
dc.language.none.fl_str_mv	eng
language	eng
dc.relation.none.fl_str_mv	info:eu-repo/semantics/altIdentifier/doi/10.1016/j.exer.2022.109353 info:eu-repo/semantics/altIdentifier/url/https://www.sciencedirect.com/science/article/pii/S0014483522004341
dc.rights.none.fl_str_mv	info:eu-repo/semantics/openAccess https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
eu_rights_str_mv	openAccess
rights_invalid_str_mv	https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
dc.format.none.fl_str_mv	application/pdf application/pdf application/pdf
dc.publisher.none.fl_str_mv	Academic Press Ltd - Elsevier Science Ltd
publisher.none.fl_str_mv	Academic Press Ltd - Elsevier Science Ltd
dc.source.none.fl_str_mv	reponame:CONICET Digital (CONICET) instname:Consejo Nacional de Investigaciones Científicas y Técnicas
reponame_str	CONICET Digital (CONICET)
collection	CONICET Digital (CONICET)
instname_str	Consejo Nacional de Investigaciones Científicas y Técnicas
repository.name.fl_str_mv	CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicas
repository.mail.fl_str_mv	dasensio@conicet.gov.ar; lcarlino@conicet.gov.ar
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score	13.070432

Molecular mechanisms regulating wound repair: Evidence for paracrine signaling from corneal epithelial cells to fibroblasts and immune cells following transient epithelial cell tre...

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