Редактирование: OSM

Oncostatin-M precursor (OSM)

==Publications==

{{medline-entry
|title=Age Differences in Sexual Minority Stress and the Importance of Friendship in Later Life.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33143546
|abstract=This study examined whether younger and middle-aged and older sexual minorities (YSM, MA[[OSM]]) experience minority stress differently in relation to social support and depressive symptomatology. Cross-sectional data from 238 sexual minorities (18-80; [i]M[/i] = 40.93) comprised the sample, who were strategically separated into cohorts. Group difference and regression methods were used to examine differences in minority stress between groups and the relationships between minority stress-social support-depressive symptomatology within groups. MA[[OSM]] had greater outness and lower IH. Additionally, outness and IH were the best predictors for the MA[[OSM]] and YSM group, respectively. MA[[OSM]] indicated better adaption to minority stresses, highlighting the importance of friend support as a protective mechanism. The minority stress-depressive symptomatology is mitigated by friend support in MA[[OSM]]. [[OSM]] and YSM demonstrate different susceptibility of minority stress on depressive symptomatology, with outness being a stronger indicator in MA[[OSM]] and IH being a stronger predictor in YSM. Social support does not work uniformly in different cohorts; however, multiple sources (i.e., family, friends) should be discussed with clients. Clinicians should treat cohort as one of the defining features of a sexual minority's lifelong experience with minority stress.

|keywords=* LGBT
* Sexual minorities
* cohort differences
* discrimination
* friendship aging
* internalized homonegativity
* minority stress
* outness
* social support
|full-text-url=https://sci-hub.do/10.1080/07317115.2020.1836107
}}
{{medline-entry
|title=Myokines as biomarkers of frailty and cardiovascular disease risk in females.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32017952
|abstract=Frailty is a risk factor for cardiovascular disease (CVD). Biomarkers have the potential to detect the early stages of frailty, such as pre-frailty. Myokines may act as biomarkers of frailty-related disease progression, as a decline in muscle health is a hallmark of the frailty phenotype. This study is a secondary analysis of 104 females 55 years of age or older with no previous history of CVD. Differences in systemic myokine concentrations based on frailty status and CVD risk profile were examined using a case-control design. Propensity matching identified two sets of 26 pairs with pre-frailty as the exposure variable in low or elevated CVD risk groups for a total 104 female participants. Frailty was assessed using the Fried Criteria (FC) and CVD risk was assessed using the Framingham Risk Score (FRS). Factorial ANOVA compared the main effects of frailty, CVD risk, and their interaction on the concentrations of 15 myokines. Differences were found when comparing elevated CVD risk status with low for the concentrations of [[EPO]] (384.76 ± 1046.07 vs. 206.63 ± 284.61 pg/mL, p = .001), [[FABP3]] (2772.61 ± 3297.86 vs. 1693.31 ± 1019.34 pg/mL, p = .017), [[FGF21]] (193.17 ± 521.09 vs. 70.18 ± 139.51 pg/mL, p = .010), IL-6 (1.73 ± 4.97 vs. 0.52 ± 0.89 pg/mL, p = .023), and IL-15 (2.62 ± 10.56 vs. 0.92 ± 1.25 pg/mL, p = .022). Pre-frail females had lower concentrations of fractalkine compared to robust (27.04 ± 20.60 vs. 103.62 ± 315.45 pg/mL, p = .004). Interaction effects between frailty status and CVD risk for [[FGF21]] and [[OSM]] were identified. In elevated CVD risk, pre-frail females, concentrations of [[FGF21]] and [[OSM]] were lower than that of elevated CVD risk, robust females (69.10 ± 62.86 vs. 317.24 ± 719.69, p = .011; 1.73 ± 2.32 vs. 24.43 ± 69.21, p = .018, respectively). These data identified specific biomarkers of CVD risk and biomarkers of frailty that are exacerbated with CVD risk.

|keywords=* Aging
* Biomarkers
* Cardiovascular disease
* Females
* Frailty
* Myokines
|full-text-url=https://sci-hub.do/10.1016/j.exger.2020.110859
}}
{{medline-entry
|title=[[STAT3]]-mediated [[SMAD3]] activation underlies Oncostatin M-induced Senescence.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/27892764
|abstract=Cytokines in the developing tumor microenvironment (TME) can drive transformation and subsequent progression toward metastasis. Elevated levels of the Interleukin-6 (IL-6) family cytokine Oncostatin M ([[OSM]]) in the breast TME correlate with aggressive, metastatic cancers, increased tumor recurrence, and poor patient prognosis. Paradoxically, [[OSM]] engages a tumor-suppressive, Signal Transducer and Activator of Transcription 3 ([[STAT3]])-dependent senescence response in normal and non-transformed human mammary epithelial cells (HMEC). Here, we identify a novel link between [[OSM]]-activated [[STAT3]] signaling and the Transforming Growth Factor-β (TGF-β) signaling pathway that engages senescence in HMEC. Inhibition of functional TGF-β/SMAD signaling by expressing a dominant-negative TGF-β receptor, treating with a TGF-β receptor inhibitor, or suppressing [[SMAD3]] expression using a [[SMAD3]]-shRNA prevented [[OSM]]-induced senescence. [[OSM]] promoted a protein complex involving activated-[[STAT3]] and [[SMAD3]], induced the nuclear localization of [[SMAD3]], and enhanced [[SMAD3]]-mediated transcription responsible for senescence. In contrast, expression of [[MYC]] (c-[[MYC]]) from a constitutive promoter abrogated senescence and strikingly, cooperated with [[OSM]] to promote a transformed phenotype, epithelial-mesenchymal transition (EMT), and invasiveness. Our findings suggest that a novel [[STAT3]]/[[SMAD3]]-signaling axis is required for [[OSM]]-mediated senescence that is coopted during the transformation process to confer aggressive cancer cell properties. Understanding how developing cancer cells bypass [[OSM]]/[[STAT3]]/[[SMAD3]]-mediated senescence may help identify novel targets for future "pro-senescence" therapies aiming to reengage this hidden tumor-suppressive response.
|mesh-terms=* Cell Nucleus
* Cellular Senescence
* Epithelial Cells
* Epithelial-Mesenchymal Transition
* Humans
* Mammary Glands, Human
* Models, Biological
* Neoplasm Invasiveness
* Oncostatin M
* Phosphorylation
* Protein Transport
* Proto-Oncogene Proteins c-myc
* Receptors, Transforming Growth Factor beta
* STAT3 Transcription Factor
* Signal Transduction
* Smad3 Protein
* Smad4 Protein
* Transcription, Genetic
|keywords=* MYC
* Oncostatin M
* SMAD3
* STAT3
* cytokine
* epithelial-mesenchymal transition
* human mammary epithelial cells
* invasion
* senescence
* transforming growth factor-β
|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5324753
}}
{{medline-entry
|title=Caenorhabditis elegans [[OSM]]-11 signaling regulates SKN-1/Nrf during embryonic development and adult longevity and stress response.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/25637691
|abstract=The Nrf family of transcription factors is critical for stress defense and detoxification. In Caenorhabditis elegans, the Nrf protein ortholog SKN-1 mediates this conserved stress response and promotes longevity. Moreover, SKN-1 is well known for its essential functions during C. elegans embryogenesis. SKN-1 is maternally deployed and initiates a signaling network specifying development of the endoderm and mesoderm. In this study, we identify the conserved Notch ligand [[OSM]]-11 as a novel regulator of SKN-1. We find that genetic inactivation of osm-11 re-establishes development of the pharynx and intestine in skn-1 deficient embryos and thereby rescues embryonic lethality associated with loss of skn-1 function. Inactivation of other DSL- and DOS-motif Notch ligands does not prevent skn-1 embryonic lethality. In addition, we show that inactivation of osm-11 in adult worms robustly enhances lifespan and promotes resistance to environmental stress. SKN-1 is required for increased longevity and heat and oxidative stress resistance but not hyperosmotic stress conferred by osm-11. [[OSM]]-11 prevents the nuclear accumulation of SKN-1 and represses the transcriptional activation of SKN-1 target genes for cellular detoxification. Our findings indicate that [[OSM]]-11 antagonizes SKN-1 during embryonic development and reveal a highly context-specific relationship between [[OSM]]-11 and SKN-1 in promoting stress resistance and longevity. 
|mesh-terms=* Aging
* Animals
* Animals, Genetically Modified
* Caenorhabditis elegans
* Caenorhabditis elegans Proteins
* DNA-Binding Proteins
* Gene Expression Regulation, Developmental
* Intracellular Signaling Peptides and Proteins
* Longevity
* Oxidative Stress
* RNA Interference
* Signal Transduction
* Transcription Factors
|keywords=* Aging
* C. elegans
* Development
* Notch signaling
* OSM-11
* SKN-1/Nrf
* Stress response
|full-text-url=https://sci-hub.do/10.1016/j.ydbio.2015.01.021
}}