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Stem cell secretome-treatment improves whole-body metabolism, reduces adiposity and promotes skeletal muscle function in aged mice

ABSTRACT: Stem cell secretome-treatment improves whole-body metabolism, reduces adiposity and promotes skeletal muscle function in aged mice

PROVIDER: PRJNA1011995 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR25880359_1.fastq.gz	Fastqsanger.gz
	SRR25880359_2.fastq.gz	Fastqsanger.gz
	SRR25880360_1.fastq.gz	Fastqsanger.gz
	SRR25880360_2.fastq.gz	Fastqsanger.gz
	SRR25880361_1.fastq.gz	Fastqsanger.gz

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Stem cell secretome-treatment improves whole-body metabolism, reduces adiposity and promotes skeletal muscle function in aged mice

Project description:Aging coincides with the progressive loss of muscle mass and strength, increased adiposity, and diminished physical function. Accordingly, interventions aimed at improving muscle, metabolic, and/or physical health are of interest to mitigate the adverse effects of aging. In this study, we tested a stem-cell secretome product which contains a host of growth, cytoskeletal remodeling, and immunomodulatory factors. We examined the effects of 4 weeks of bi-weekly unilateral intramuscular secretome injections (quadriceps) in ambulatory aged male C57Bl/6 mice (22-23 months) compared to saline injected aged-matched controls. After 4 weeks of treatment, secretome delivery substantially increased whole body lean mass and decreased fat mass corresponding to higher fiber cross sectional area and smaller adipocyte size, respectively. Secretome-treated mice also displayed improved whole-body grip strength and rotarod performance and had higher energy expenditure and physical activity levels compared to control mice. Furthermore, secretome-treated mice had greater skeletal muscle Pax7+ cell abundance, capillary density, and collagen turnover. Finally, the secretome product reduced lipid content and lipid droplet size in adipocytes in vitro. These data suggest intramuscular treatment secretome improves whole-body metabolism, physical function, and remodels skeletal muscle and adipose tissue in aged mice.

2024-07-31 | GSE242211 | GEO

Stem cell secretome treatment improves whole-body metabolism, reduces adiposity, and promotes skeletal muscle function in aged mice.

Project description:Aging coincides with the progressive loss of muscle mass and strength, increased adiposity, and diminished physical function. Accordingly, interventions aimed at improving muscle, metabolic, and/or physical health are of interest to mitigate the adverse effects of aging. In this study, we tested a stem cell secretome product, which contains extracellular vesicles and growth, cytoskeletal remodeling, and immunomodulatory factors. We examined the effects of 4 weeks of 2×/week unilateral intramuscular secretome injections (quadriceps) in ambulatory aged male C57BL/6 mice (22-24 months) compared to saline-injected aged-matched controls. Secretome delivery substantially increased whole-body lean mass and decreased fat mass, corresponding to higher myofiber cross-sectional area and smaller adipocyte size, respectively. Secretome-treated mice also had greater whole-body physical function (grip strength and rotarod performance) and had higher energy expenditure and physical activity levels compared to control mice. Furthermore, secretome-treated mice had greater skeletal muscle Pax7+ cell abundance, capillary density, collagen IV turnover, reduced intramuscular lipids, and greater Akt and hormone sensitive lipase phosphorylation in adipose tissue. Finally, secretome treatment in vitro directly enhanced muscle cell growth and IL-6 production, and in adipocytes, it reduced lipid content and improved insulin sensitivity. Moreover, indirect treatment with secretome-treated myotube culture media also enhanced muscle cell growth and adipocyte size reduction. Together, these data suggest that intramuscular treatment with a stem cell secretome improves whole-body metabolism, physical function, and remodels skeletal muscle and adipose tissue in aged mice.

| S-EPMC11296109 | biostudies-literature

CIDR_Visceral Adiposity

Project description:CIDR_Visceral Adiposity

| PRJNA75481 | ENA

Topical ABT-263 treatment reduces aged skin senescence and improves subsequent wound healing

Project description:Topical ABT-263 treatment reduces aged skin senescence and improves subsequent wound healing

| PRJNA1130066 | ENA

Topical ABT-263 treatment reduces aged skin senescence and improves subsequent wound healing

Project description:Senescent cells accumulate in aging tissues, impairing their ability to undergo repair and regeneration following injury. Previous research has demonstrated that targeting tissue senescence with senolytics can enhance tissue regeneration and repair by selectively eliminating senescent cells in specific aged tissues. In this study, we focused on eliminating senescent skin cells in aged mice to assess the effects on subsequent wound healing. We applied ABT-263 (Navitoclax) and a DMSO control directly to the skin of 24-month-old mice over a 5-day period. Following ABT-263 treatment, aged skin showed decreased gene expression of senescent markers p16 and p21, accompanied by reductions in SA-β-gal and p21-positive cells compared to the DMSO-treated skin. However, ABT-263 treatment also triggered a temporary inflammatory response and macrophage infiltration in the skin. Bulk RNA sequencing of ABT-263-treated skin revealed prompt upregulation of genes associated with wound healing pathways, including hemostasis, inflammation, cell proliferation, angiogenesis, collagen synthesis, and extracellular matrix organization. Aged mice treated with ABT-263 exhibited accelerated wound closure compared to the DMSO control group. In conclusion, topical ABT-263 effectively reduced several senescence markers in aged skin, thereby priming the skin for improved subsequent wound healing. This enhancement may be attributed to ABT-263-induced senolysis and the resulting inflammation, which in turn stimulated the expression of genes involved in extracellular matrix remodeling and wound repair pathways.

2024-12-17 | GSE271149 | GEO

Induced Mesenchymal stromal cells derived from iPS cells from aged individuals acquire a rejuvenation signature and a MSC-specific secretome

Project description:Human induced pluripotent stem cells (iPSCs) - derived mesenchymal stromal cells (iMSCs) are a potentially useful cell type for circumventing ageing-related shortfalls associated with primary mesenchymal or skeletal stromal cells (MSCs/SSCs). To date, the extent of the reflection of ageing-hallmarks in iMSCs differentiated from iPSCs derived from elderly donors remains unclear. In this study, we show that fetal (55 days post conception) femur-derived MSCs and MSCs isolated from aged (60 – 74 years) donors differ in their transcriptome and secretome profile. Yet, iMSCs irrespective of donor age and cell type acquired a rejuvenation gene signature, specifically, INHBE, DNMT3B, POU5F1P1, CDKN1C, GCNT2; also present in pluripotent stem cells but not observed in the parental MSCs. Furthermore, dendrograms generated from the transcriptomes of iMSCs derived from the human embryonic stem cell line H1, fetal and aged MSCs always clustered together with the parental fetal femur-derived MSCs. In addition, these were distinct from MSCs isolated from aged donors when comparing gene ontologies (GOs) related to ageing processes. Critically, in terms of regenerative medicine applications, iMSCs re-acquired a similar secretome (e.g. SERPINE1, SDF-1a, HGF, IL6, IL10, THBS1) to that of the parental fetal MSCs, thus re-enforcing their capabilities of imparting context dependent paracrine signaling.

2019-03-13 | GSE97311 | GEO

Hepatocyte‑specific Ccnd1 knockout in aged mice reduces inflammatory signaling

Project description:Hepatocyte‑specific Ccnd1 knockout in aged mice reduces inflammatory signaling

| PRJNA1299809 | ENA

GRSF1 deficiency in skeletal muscle reduces endurance in aged mice

Project description:GRSF1 deficiency in skeletal muscle reduces endurance in aged mice

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Growth hormone supplementation reduces aneuploidy and improves the quality of oocytes by activating ERK1/2 pathway in aged mice

Project description:The decline in oocyte quality is a limiting factor of female fertility; however, strategies to maintain the oocyte quality of aged women are not available. In this study, we showed that growth hormone (GH) supplementation in vivo not only alleviated the decline in oocyte number caused by aging, but also improved the quality and developmental potential of aged oocytes. Strikingly, GH supplementation reduced aneuploidy in aged oocytes. Proteomic analysis indicated that the ERK1/2 pathway was involved in the reduction in aneuploidy rate of aged oocytes, as confirmed both in vivo and in vitro. In addition, JAK2 might be involved in the regulation of ERK1/2 by GH in aged oocytes. Collectively, our findings revealed that GH supplementation protects oocytes from aging-related aneuploidy and enhances the quality of aged oocytes, and could be used to improve the outcome of assisted reproduction in aged women.

2023-07-20 | PXD039147 | Pride

Conjugated linoleic acid activates AMPK and reduces adiposity more effectively when used with metformin

Project description:Trans-10, cis-12 conjugated linoleic acid (t10c12 CLA) causes dramatic reductions in white adipose tissue in mice but has had limited effectiveness in humans. Determination of the signaling pathways involved may lead to better regulation of adiposity. T10c12 CLA was found to activate AMP-activating protein kinase (AMPK), a central regulator of cell metabolism. Compound C, a potent inhibitor of AMPK, prevents many of the typical responses to treatments with t10c12 CLA including the integrated stress response (ISR), the inflammatory response, the reduction in key lipogenic transcription factors, and delipidation. Treatment of adipocytes or mice with t10c12 CLA in conjunction with AMPK activator metformin results in more delipidation than treatment with the individual chemicals. Additionally, the combination showed a reduced inflammatory response relative to a t10c12 CLA treatment alone. The combination of t10c12 CLA and metformin, widely used to treat insulin resistance and Type II diabetes, has potential as a treatment for reducing adiposity in humans. Keywords: control/treatment Mouse 3T3-L1 RNA for was isolated from control linoleic acid (LA) and treatment (CLA, CLA+metformin, metformin) samples for analysis on microarrays with three biological reps.

2009-11-01 | E-GEOD-14888 | biostudies-arrayexpress

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