Engineered Enucleated Mesenchymal Stem Cells Regulating Immune Microenvironment and Promoting Wound Healing
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ABSTRACT:
ORGANISM(S): Mus
PROVIDER: GSE283228 | GEO | 2025/12/16
REPOSITORIES: GEO
Similar Datasets
Project description:Wound healing is a multi-step process to rapidly restore barrier function. This process is often impaired in diabetic patients resulting in chronic wounds and amputation. We previously found that paradoxical activation of the mitogen-activated protein kinase (MAPK) pathway via topical administration of the BRAF inhibitor vemurafenib accelerates wound healing by activating keratinocyte proliferation and reepithelialization pathways in healthy mice. Herein, we investigated whether this wound healing acceleration also occurs in impaired diabetic wounds and found that topical vemurafenib not only improves wound healing in a murine diabetic wound model, but unexpectedly promotes hair follicle regeneration. Neogenic hair follicles expressing Sox-9, CD34 and K15 were found in wounds of diabetic and non-diabetic mice, and their formation can be prevented by blocking downstream MEK signaling. Thus, topically applied BRAF inhibitors may accelerate wound healing, and promote the restoration of improved skin architecture in both normal and impaired wounds.
2021-05-22 | GSE148037 | GEO
Project description:Clinical skin manifestations are common in diabetes; however, molecular mechanisms underlying such defects are largely unknown. Several findings indicate a role for microRNA (miRNA) in skin homeostasis. We investigated whether miRNA expression is altered in the skin of a Type 1 mouse model of diabetes. For this purpose, miRNA profiling by microarray analysis was performed on RNA extracted from the skin of diabetic mice and non-diabetic controls. >400 different miRNA species were identified, differential expression-analysis revealed miRNA dysregulation in diabetic skin. Interestingly, among the 30 most significantly modulated genes, 27 were downregulated and 3 were upregulated in diabetic mice. Pathway analysis using Tarbase showed an enrichment of signature-miRNA target genes in pathways with roles in skin homeostasis, such as TGF-β and Wnt.
2020-07-10 | GSE137605 | GEO
Project description:The Janus liposozyme robustly eradicates infections and rapidly promotes wound closure and re-epithelialization on diabetic skin wound infected with methicillin-resistant S. aureus (MRSA). We used single cell RNA sequencing(scRNA-seq) to deep analyse local immune homeostasis manipulated by Janus on skin cells obtained from db/db mice .
2024-01-17 | GSE253098 | GEO
Project description:This a model from the article:
Modeling the effects of treating diabetic wounds with engineered skin
substitutes.
Waugh HV, Sherratt JA. Wound Repair Regen
2007 Jul-Aug;15(4):556-65 17650100
,
Abstract:
In this paper, a novel mathematical model of wound healing in both normal and
diabetic cases is presented, focusing upon the effects of adding two currently
available commercial engineered skin substitute therapies to the wound
(Apligraf) and Dermagraft). Our work extends a previously developed model, which
considers inflammatory and repair macrophage dynamics in normal and diabetic
wound healing. Here, we extend the model to include equations for
platelet-derived growth factor concentration, fibroblast density, collagen
density, and hyaluronan concentration. This enables us to examine the variation
of these components in both normal and diabetic wound healing cases, and to
model the treatment protocols of these therapies. Within the context of our
model, we find that the key component to successful healing in diabetic wounds
is hyaluronan and that the therapies work by increasing the amount of hyaluronan
available in the wound environment. The time-to-healing results correlate with
those observed in clinical trials and the model goes some way to establishing an
understanding of why diabetic wounds do not heal, and how these treatments
affect the diabetic wound environment to promote wound closure.
This model was taken from the CellML repository
and automatically converted to SBML.
The original model was:
Waugh HV, Sherratt JA. (2007) - version=1.0
The original CellML model was created by:
Catherine Lloyd
c.lloyd@auckland.ac.nz
The University of Auckland
This model originates from BioModels Database: A Database of Annotated Published Models (http://www.ebi.ac.uk/biomodels/). It is copyright (c) 2005-2011 The BioModels.net Team.
To the extent possible under law, all copyright and related or neighbouring rights to this encoded model have been dedicated to the public domain worldwide. Please refer to CC0 Public Domain Dedication
for more information.
In summary, you are entitled to use this encoded model in absolutely any manner you deem suitable, verbatim, or with modification, alone or embedded it in a larger context, redistribute it, commercially or not, in a restricted way or not..
To cite BioModels Database, please use: Li C, Donizelli M, Rodriguez N, Dharuri H, Endler L, Chelliah V, Li L, He E, Henry A, Stefan MI, Snoep JL, Hucka M, Le Novère N, Laibe C (2010) BioModels Database: An enhanced, curated and annotated resource for published quantitative kinetic models. BMC Syst Biol., 4:92.
2005-01-01 | MODEL1006230003 | BioModels
Project description:This a model from the article:
Modeling the effects of treating diabetic wounds with engineered skin
substitutes.
Waugh HV, Sherratt JA. Wound Repair Regen
2007 Jul-Aug;15(4):556-65 17650100
,
Abstract:
In this paper, a novel mathematical model of wound healing in both normal and
diabetic cases is presented, focusing upon the effects of adding two currently
available commercial engineered skin substitute therapies to the wound
(Apligraf) and Dermagraft). Our work extends a previously developed model, which
considers inflammatory and repair macrophage dynamics in normal and diabetic
wound healing. Here, we extend the model to include equations for
platelet-derived growth factor concentration, fibroblast density, collagen
density, and hyaluronan concentration. This enables us to examine the variation
of these components in both normal and diabetic wound healing cases, and to
model the treatment protocols of these therapies. Within the context of our
model, we find that the key component to successful healing in diabetic wounds
is hyaluronan and that the therapies work by increasing the amount of hyaluronan
available in the wound environment. The time-to-healing results correlate with
those observed in clinical trials and the model goes some way to establishing an
understanding of why diabetic wounds do not heal, and how these treatments
affect the diabetic wound environment to promote wound closure.
This model was taken from the CellML repository
and automatically converted to SBML.
The original model was:
Waugh HV, Sherratt JA. (2007) - version=1.0
The original CellML model was created by:
Catherine Lloyd
c.lloyd@auckland.ac.nz
The University of Auckland
This model originates from BioModels Database: A Database of Annotated Published Models (http://www.ebi.ac.uk/biomodels/). It is copyright (c) 2005-2011 The BioModels.net Team.
To the extent possible under law, all copyright and related or neighbouring rights to this encoded model have been dedicated to the public domain worldwide. Please refer to CC0 Public Domain Dedication
for more information.
In summary, you are entitled to use this encoded model in absolutely any manner you deem suitable, verbatim, or with modification, alone or embedded it in a larger context, redistribute it, commercially or not, in a restricted way or not..
To cite BioModels Database, please use: Li C, Donizelli M, Rodriguez N, Dharuri H, Endler L, Chelliah V, Li L, He E, Henry A, Stefan MI, Snoep JL, Hucka M, Le Novère N, Laibe C (2010) BioModels Database: An enhanced, curated and annotated resource for published quantitative kinetic models. BMC Syst Biol., 4:92.
2005-01-01 | MODEL1006230099 | BioModels
Project description:This a model from the article:
Modeling the effects of treating diabetic wounds with engineered skin
substitutes.
Waugh HV, Sherratt JA. Wound Repair Regen
2007 Jul-Aug;15(4):556-65 17650100
,
Abstract:
In this paper, a novel mathematical model of wound healing in both normal and
diabetic cases is presented, focusing upon the effects of adding two currently
available commercial engineered skin substitute therapies to the wound
(Apligraf) and Dermagraft). Our work extends a previously developed model, which
considers inflammatory and repair macrophage dynamics in normal and diabetic
wound healing. Here, we extend the model to include equations for
platelet-derived growth factor concentration, fibroblast density, collagen
density, and hyaluronan concentration. This enables us to examine the variation
of these components in both normal and diabetic wound healing cases, and to
model the treatment protocols of these therapies. Within the context of our
model, we find that the key component to successful healing in diabetic wounds
is hyaluronan and that the therapies work by increasing the amount of hyaluronan
available in the wound environment. The time-to-healing results correlate with
those observed in clinical trials and the model goes some way to establishing an
understanding of why diabetic wounds do not heal, and how these treatments
affect the diabetic wound environment to promote wound closure.
This model was taken from the CellML repository
and automatically converted to SBML.
The original model was:
Waugh HV, Sherratt JA. (2007) - version=1.0
The original CellML model was created by:
Catherine Lloyd
c.lloyd@auckland.ac.nz
The University of Auckland
This model originates from BioModels Database: A Database of Annotated Published Models (http://www.ebi.ac.uk/biomodels/). It is copyright (c) 2005-2011 The BioModels.net Team.
To the extent possible under law, all copyright and related or neighbouring rights to this encoded model have been dedicated to the public domain worldwide. Please refer to CC0 Public Domain Dedication
for more information.
In summary, you are entitled to use this encoded model in absolutely any manner you deem suitable, verbatim, or with modification, alone or embedded it in a larger context, redistribute it, commercially or not, in a restricted way or not..
To cite BioModels Database, please use: Li C, Donizelli M, Rodriguez N, Dharuri H, Endler L, Chelliah V, Li L, He E, Henry A, Stefan MI, Snoep JL, Hucka M, Le Novère N, Laibe C (2010) BioModels Database: An enhanced, curated and annotated resource for published quantitative kinetic models. BMC Syst Biol., 4:92.
2005-01-01 | MODEL1006230102 | BioModels
Project description:This a model from the article:
Modeling the effects of treating diabetic wounds with engineered skin
substitutes.
Waugh HV, Sherratt JA. Wound Repair Regen
2007 Jul-Aug;15(4):556-65 17650100
,
Abstract:
In this paper, a novel mathematical model of wound healing in both normal and
diabetic cases is presented, focusing upon the effects of adding two currently
available commercial engineered skin substitute therapies to the wound
(Apligraf) and Dermagraft). Our work extends a previously developed model, which
considers inflammatory and repair macrophage dynamics in normal and diabetic
wound healing. Here, we extend the model to include equations for
platelet-derived growth factor concentration, fibroblast density, collagen
density, and hyaluronan concentration. This enables us to examine the variation
of these components in both normal and diabetic wound healing cases, and to
model the treatment protocols of these therapies. Within the context of our
model, we find that the key component to successful healing in diabetic wounds
is hyaluronan and that the therapies work by increasing the amount of hyaluronan
available in the wound environment. The time-to-healing results correlate with
those observed in clinical trials and the model goes some way to establishing an
understanding of why diabetic wounds do not heal, and how these treatments
affect the diabetic wound environment to promote wound closure.
This model was taken from the CellML repository
and automatically converted to SBML.
The original model was:
Waugh HV, Sherratt JA. (2007) - version=1.0
The original CellML model was created by:
Catherine Lloyd
c.lloyd@auckland.ac.nz
The University of Auckland
This model originates from BioModels Database: A Database of Annotated Published Models (http://www.ebi.ac.uk/biomodels/). It is copyright (c) 2005-2011 The BioModels.net Team.
To the extent possible under law, all copyright and related or neighbouring rights to this encoded model have been dedicated to the public domain worldwide. Please refer to CC0 Public Domain Dedication
for more information.
In summary, you are entitled to use this encoded model in absolutely any manner you deem suitable, verbatim, or with modification, alone or embedded it in a larger context, redistribute it, commercially or not, in a restricted way or not..
To cite BioModels Database, please use: Li C, Donizelli M, Rodriguez N, Dharuri H, Endler L, Chelliah V, Li L, He E, Henry A, Stefan MI, Snoep JL, Hucka M, Le Novère N, Laibe C (2010) BioModels Database: An enhanced, curated and annotated resource for published quantitative kinetic models. BMC Syst Biol., 4:92.
2005-01-01 | MODEL1006230106 | BioModels
Project description:To investigate how HOXA3 expression in wound tissue alters gene expression to control selective recruitment of bone marrow-derived cell populations, we utilized murine whole genome expression arrays (MEEBO arrays) to identify differentially expressed genes in cutaneous wounds from db/db (diabetic) mice treated with either CMV-HOXA3 or control plasmid. In addition to unwounded control skin, we chose day 4 as the time point to harvest the wounds for RNA isolation, which represents the transition from inflammatory to proliferative phase of wound repair, and precedes the observed differences in BMDC mobilization and recruitment at day 7. Set of arrays organized by shared biological context, such as organism, tumors types, processes, etc. Disease State: cutaneous wound/control skin unwounded skin, wounded skin treated with control plasmid, wounded skin treated with HOXA3
2009-10-12 | E-GEOD-13324 | biostudies-arrayexpress
Project description:MiR-132 is one of the most upregulated miRNAs in human skin wounds at the inflammatory phase of healing. MiR-132 inhibits inflammation but promotes growth of epidermal keratinocytes, indicating that it may facilitate the inflammatory-proliferative phase transition during wound repair. Following this line of research, here we evaluated the therapeutic potential of miR-132 in chronic wound using mouse in vivo wound model. We performed a global transcriptome analysis of skin wounds of leptin receptor-deficient (db/db) mice treated with miR-132 or control mimics. Db/db mouse has been used as a type 2 diabetic model with impaired wound healing capacity.
2017-02-01 | GSE92409 | GEO
Project description:Objective This study aims to investigate the effects of electroacupuncture on chronic wounds associated with diabetes, particularly focusing on its potential mechanisms for enhancing wound healing through the promotion of angiogenesis. While acupuncture has been shown to improve wound healing by enhancing blood supply and vascular regeneration, the therapeutic effects of electroacupuncture in diabetic chronic wounds have not been sufficiently addressed. Methods A diabetic skin ulcer mouse model was established for this study. The effects of electroacupuncture on wound healing were assessed through evaluation of skin healing rates, ELISA assays, and histopathological analyses. Additionally, a tissue transparency three-dimensional imaging technique was utilized to establish a vascular model of wounds on day 10, clarifying the impact of electroacupuncture on angiogenesis during the proliferation phase in diabetic mouse skin wound models. Proteomic analysis was conducted to identify potential targets and mechanisms by which electroacupuncture regulates diabetic wound healing, further validated by immunohistochemistry (IHC) and Western blotting (WB). Results The experimental results demonstrated that electroacupuncture significantly promotes wound healing in diabetic mice, reduces the levels of the pro-inflammatory cytokine IL-6 during the inflammatory phase, decreases inflammatory cell infiltration, and increases collagen synthesis. Proteomic analysis indicated that electroacupuncture may facilitate diabetic wound healing by enhancing endothelial cell proliferation and modulating angiogenic morphogenesis. Furthermore, electroacupuncture was shown to upregulate the expression of CXCL12 and its co-localization with CXCR4, while promoting the phosphorylation of PI3K and AKT, thereby enhancing the expression of VEGF and improving angiogenesis. Three-dimensional tissue transparency imaging provided comprehensive visual evidence of the angiogenic effects induced by electroacupuncture. Conclusion The findings of this study suggest that electroacupuncture activates the PI3K/AKT signaling pathway through the CXCL12/CXCR4 axis to promote vascular regeneration, thereby improving the healing process of diabetic skin wounds in mice.
2024-12-26 | PXD059248 |