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Multistep analysis of type I collagen synthesis and the effects of 4-phenylbutyric acid in patients with osteogenesis imperfecta-derived cells

ABSTRACT: We performed shotgun proteomic analysis of human type I collagen purified from the culture medium of normal or osteogenesis imperfecta fibroblasts by LC-MS after trypsin digestion for identification of lysine glycosylation sites.

ORGANISM(S): Homo Sapiens (human)

SUBMITTER: Takuo Kubota

PROVIDER: PXD021411 | JPOST Repository | Fri Feb 05 00:00:00 GMT 2021

REPOSITORIES: jPOST

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			Action	DRS
	Normal.baf	Other
	Normal.group	Other
	Normal_PeptideSummary.txt	Txt
	Normal_ProteinSummary.txt	Txt
	Nromal.mgf	Mgf

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Effects of O2 concentration on endeometrial organoids within collagen-based gel (70% type I collagen and 30% matrigel)

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Effects of human collagen α-1 type I-derived proteins on collagen synthesis and elastin production in human dermal fibroblasts.

Project description:Collagen type I is the most abundant form of collagen in human tissues, and is composed of two identical α-1 type I chains and an α-2 type I chain organized in a triple helical structure. A previous study has shown that human collagen α-2 type I (hCOL1A2) promotes collagen synthesis, wound healing, and elastin production in normal human dermal fibroblasts (HDFs). However, the biological effects of human collagen α-1 type I (hCOL1A1) on various skin properties have not been investigated. Here, we isolate and identify the hCOL1A1-collagen effective domain (CED) which promotes collagen type I synthesis. Recombinant hCOL1A1-CED effectively induces cell proliferation and collagen biosynthesis in HDFs, as well as increased cell migration and elastin production. Based on these results, hCOL1A1-CED may be explored further for its potential use as a preventative agent against skin aging. [BMB Reports 2021; 54(6): 329-334].

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iPSC-derived type IV collagen α5-expressing kidney organoids model Alport syndrome

Project description:Alport syndrome (AS) is a hereditary glomerulonephritis caused by COL4A3, COL4A4 or COL4A5 gene mutations and characterized by abnormalities of glomerular basement membranes (GBMs). Due to a lack of curative treatments, the condition proceeds to end-stage renal disease even in adolescents. Hampering drug discovery is the absence of effective in vitro methods for testing the restoration of normal GBMs. Here, we aimed to develop kidney organoid models from AS patient iPSCs for this purpose. We established iPSC-derived collagen α5(IV)-expressing kidney organoids and confirmed that kidney organoids from COL4A5 mutation-corrected iPSCs restore collagen α5(IV) protein expression. Importantly, our model recapitulates the differences in collagen composition between iPSC-derived kidney organoids from mild and severe AS cases. Furthermore, we demonstrate that a chemical chaperone, 4-phenyl butyric acid, has the potential to correct GBM abnormalities in kidney organoids showing mild AS phenotypes. This iPSC-derived kidney organoid model will contribute to drug discovery for AS.

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Effects of O2 concentration on endeometrial organoids within collagen-based gel (70% type I collagen and 30% matrigel)

Project description:Effects of O2 concentration on endeometrial organoids within collagen-based gel (70% type I collagen and 30% matrigel)

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Near-infrared-emitting nanoparticles activate collagen synthesis via TGFβ signaling

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Tumor-associated macrophages derived from circulating inflammatory monocytes degrade collagen through cellular uptake

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The m6A writer KIAA1429 regulates photoaging progression via MFAP4-dependent collagen synthesis

Project description:Background: N6-Methyladenosine (m6A) methylation, a common form of RNA modification, play an important role in the pathogenesis of various diseases and in the ontogeny of organisms. Nevertheless, the precise function of m6A methylation in photoaging remains unknown. Objectives: This study aims to investigate the biological role and underlying mechanism of m6A methylation in photoaging. Methods: m6A dot blot, Real-time quantitative PCR (RT-qPCR), western blot and immunohistochemical (IHC) assays were employed to detect the m6A level and specific m6A methylase in ultraviolet ray (UVR)-induced photoaging tissue. The profile of m6A-tagged mRNA was identified by methylated RNA immunoprecipitation sequencing (MeRIP-seq) and RNA-seq analysis. Finally, we investigated the regulatory mechanism of KIAA1429 by MeRIP-qPCR, RNA knockdown and immunofluorescence assay. Results: m6A levels were increased in photoaging and were closely associated with the upregulation of KIAA1429 expression. 1331 differentially m6A methylated genes were identified in the UVR group compared with the control group, of which 1192 (90%) were hypermethylated. Gene ontology analysis showed that genes with m6A hypermethylation and mRNA downregulation were mainly involved in extracellular matrix metabolism and collagen metabolism-related processes. Furthermore, KIAA1429 knockdown abolished the downregulation of TGF-R and upregulation of MMP1 in UVR-irradiated HDFs. Mechanically, we identified MFAP4 as a target of KIAA1429-mediated m6A modification and KIAA1429 might suppress collagen synthesis through an m6A-MFAP4-mediated process. Conclusions: The increased expression of KIAA1429 hinders collagen synthesis during UVR-induced photoaging, suggesting that KIAA1429 represents a potential candidate for targeted therapy to mitigate UVR-driven photoaging.

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