RNAseq of TGF-β receptor type I kinase-dependent genes in oral fibroblast exposed to milk

Abstract Background Milk is a rich source of natural growth factors that may support oral tissue homeostasis and wound healing. We had shown earlier that blocking TGF-β receptor type I kinase with the inhibitor SB431542 abolished the expression of IL11 and other genes in human gingival fibroblasts e...

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Autores principales:	Layla Panahipour, Dariush Mehdipour Moghaddam, Jila Nasirzade, Zahra Kargarpour, Reinhard Gruber
Formato:	article
Lenguaje:	EN
Publicado:	BMC 2021
Materias:	Human milk TGF-β activity TGF-β receptor type I kinase Gingival fibroblast In vitro Dentistry RK1-715
Acceso en línea:	https://doaj.org/article/2627b7764bfd41ffa498f85c5d02189b
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spelling	oai:doaj.org-article:2627b7764bfd41ffa498f85c5d02189b2021-11-21T12:32:18ZRNAseq of TGF-β receptor type I kinase-dependent genes in oral fibroblast exposed to milk10.1186/s12903-021-01913-51472-6831https://doaj.org/article/2627b7764bfd41ffa498f85c5d02189b2021-11-01T00:00:00Zhttps://doi.org/10.1186/s12903-021-01913-5https://doaj.org/toc/1472-6831Abstract Background Milk is a rich source of natural growth factors that may support oral tissue homeostasis and wound healing. We had shown earlier that blocking TGF-β receptor type I kinase with the inhibitor SB431542 abolished the expression of IL11 and other genes in human gingival fibroblasts exposed to the aqueous fraction of milk. Our aim was to identify the entire signature of TGF-β receptor type I kinase-dependent genes regulated by the aqueous fraction of human milk. Result RNAseq revealed 99 genes being strongly regulated by milk requiring activation of the SB431542-dependent TGF-β receptor type I kinase. Among the SB431542-dependent genes is IL11 but also cadherins, claudins, collagens, potassium channels, keratins, solute carrier family proteins, transcription factors, transmembrane proteins, tumor necrosis factor ligand superfamily members, and tetraspanin family members. When focusing on our candidate gene, we could identify D609 to suppress IL11 expression, independent of phospholipase C, sphinosine-1 phosphate synthesis, and Smad-3 phosphorylation and its nuclear translocation. In contrast, genistein and blocking phosphoinositide 3-kinases by wortmannin and LY294002 increased the milk-induced IL11 expression in gingival fibroblasts. Conclusion Taken together, our data revealed TGF-β receptor type I kinase signaling to cause major changes of the genetic signature of gingival fibroblasts exposed to aqueous fraction of human milk.Layla PanahipourDariush Mehdipour MoghaddamJila NasirzadeZahra KargarpourReinhard GruberBMCarticleHuman milkTGF-β activityTGF-β receptor type I kinaseGingival fibroblastIn vitroDentistryRK1-715ENBMC Oral Health, Vol 21, Iss 1, Pp 1-9 (2021)
institution	DOAJ
collection	DOAJ
language	EN
topic	Human milk TGF-β activity TGF-β receptor type I kinase Gingival fibroblast In vitro Dentistry RK1-715
spellingShingle	Human milk TGF-β activity TGF-β receptor type I kinase Gingival fibroblast In vitro Dentistry RK1-715 Layla Panahipour Dariush Mehdipour Moghaddam Jila Nasirzade Zahra Kargarpour Reinhard Gruber RNAseq of TGF-β receptor type I kinase-dependent genes in oral fibroblast exposed to milk
description	Abstract Background Milk is a rich source of natural growth factors that may support oral tissue homeostasis and wound healing. We had shown earlier that blocking TGF-β receptor type I kinase with the inhibitor SB431542 abolished the expression of IL11 and other genes in human gingival fibroblasts exposed to the aqueous fraction of milk. Our aim was to identify the entire signature of TGF-β receptor type I kinase-dependent genes regulated by the aqueous fraction of human milk. Result RNAseq revealed 99 genes being strongly regulated by milk requiring activation of the SB431542-dependent TGF-β receptor type I kinase. Among the SB431542-dependent genes is IL11 but also cadherins, claudins, collagens, potassium channels, keratins, solute carrier family proteins, transcription factors, transmembrane proteins, tumor necrosis factor ligand superfamily members, and tetraspanin family members. When focusing on our candidate gene, we could identify D609 to suppress IL11 expression, independent of phospholipase C, sphinosine-1 phosphate synthesis, and Smad-3 phosphorylation and its nuclear translocation. In contrast, genistein and blocking phosphoinositide 3-kinases by wortmannin and LY294002 increased the milk-induced IL11 expression in gingival fibroblasts. Conclusion Taken together, our data revealed TGF-β receptor type I kinase signaling to cause major changes of the genetic signature of gingival fibroblasts exposed to aqueous fraction of human milk.
format	article
author	Layla Panahipour Dariush Mehdipour Moghaddam Jila Nasirzade Zahra Kargarpour Reinhard Gruber
author_facet	Layla Panahipour Dariush Mehdipour Moghaddam Jila Nasirzade Zahra Kargarpour Reinhard Gruber
author_sort	Layla Panahipour
title	RNAseq of TGF-β receptor type I kinase-dependent genes in oral fibroblast exposed to milk
title_short	RNAseq of TGF-β receptor type I kinase-dependent genes in oral fibroblast exposed to milk
title_full	RNAseq of TGF-β receptor type I kinase-dependent genes in oral fibroblast exposed to milk
title_fullStr	RNAseq of TGF-β receptor type I kinase-dependent genes in oral fibroblast exposed to milk
title_full_unstemmed	RNAseq of TGF-β receptor type I kinase-dependent genes in oral fibroblast exposed to milk
title_sort	rnaseq of tgf-β receptor type i kinase-dependent genes in oral fibroblast exposed to milk
publisher	BMC
publishDate	2021
url	https://doaj.org/article/2627b7764bfd41ffa498f85c5d02189b
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RNAseq of TGF-β receptor type I kinase-dependent genes in oral fibroblast exposed to milk

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