Редактирование: TGFB1

Transforming growth factor beta-1 proprotein precursor [Contains: Latency-associated peptide (LAP); Transforming growth factor beta-1 (TGF-beta-1)] [TGFB]

==Publications==

{{medline-entry
|title=Different expression of Defensin-B gene in the endometrium of mares of different age during the breeding season.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31864349
|abstract=Despite being one of the major causes of infertility in mares, the mechanisms responsible for equine endometrosis are still unclear and controversial. In the last few years, many investigations focused on local immune response modulation. Since it is generally accepted that endometrial fibrosis increases with age, we hypothesize that older mares could show altered local immune modulation, initiating a pro-inflammatory and tissue remodeling cascade of events that could lead to endometrosis. The aim of this study, indeed, is to evaluate and describe the local gene expression of genes involved in acute inflammatory response and fibrosis (COL1A1, [[COL3A1]], TNFA, [[MMP9]], [[IL6]], [[TGFB1]] and TGFBR1), together with others associated to immune modulation ([[DEFB4B]], [[IDO1]] and [[FOXP3]]), in uterine specimens from mares of different age. Twenty-five Standardbred mares were involved in the study with age ranging from 7 to 19 years (mean 10.40 ± 4.42). They were divided by age into two groups: G1 (n = 15, less than 10 years old) and G2 (N = 10, greater than 11 years old). Specimens from the uterus' right horn-body junction were collected and processed for histology evaluation and RT-qPCR assay.Gene expression of [[DEFB4B]], [[MMP9]] and TNFA was higher in younger mares, suggesting a balance in immune modulation and tissue remodeling. Interleukin-6 and [[COL3A1]] gene expressions were greater in older animals, probably indicating inflammatory pathways activation and fibrosis increase. Although no differences in fibrosis and inflammation distribution could be found with histological examination among G1 and G2, our results suggest a possible involvement of DEF4BB in regulating the local immune response in younger mare's uterus (G1); age may contribute to the dis-regulation of [[DEFB4B]] transcription and, indirectly, influence the extracellular matrix homeostasis. Transcription of [[IDO1]] and [[FOXP3]] genes, instead, does not seem to be age related, or to be involved in local immune-response and tissue remodeling functions. Further investigations are needed in order to clarify the interactions between the expression of [[DEFB4B]], [[IL6]], TNFA, [[COL3A1]] and [[MMP9]] and other local signals of immune-modulation and tissue remodeling, in mares in a prospective study design.
|mesh-terms=* Aging
* Animals
* Breeding
* Defensins
* Endometrium
* Female
* Fibrosis
* Gene Expression
* Horses
* Inflammation
* Reverse Transcriptase Polymerase Chain Reaction
|keywords=* Defensin-β
* Endometrium
* Gene expression
* Immune-modulation
* Mare
|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6925900
}}
{{medline-entry
|title=[[TGFB1]]-Mediated Gliosis in Multiple Sclerosis Spinal Cords Is Favored by the Regionalized Expression of [[HOXA5]] and the Age-Dependent Decline in Androgen Receptor Ligands.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31779094
|abstract=In multiple sclerosis (MS) patients with a progressive form of the disease, spinal cord (SC) functions slowly deteriorate beyond age 40. We previously showed that in the SC of these patients, large areas of incomplete demyelination extend distance away from plaque borders and are characterized by a unique progliotic [[TGFB1]] (Transforming Growth Factor Beta 1) genomic signature. Here, we attempted to determine whether region- and age-specific physiological parameters could promote the progression of SC periplaques in MS patients beyond age 40. An analysis of transcriptomics databases showed that, under physiological conditions, a set of 10 homeobox (HOX) genes are highly significantly overexpressed in the human SC as compared to distinct brain regions. Among these HOX genes, a survey of the human proteome showed that only [[HOXA5]] encodes a protein which interacts with a member of the TGF-beta signaling pathway, namely [[SMAD1]] (SMAD family member 1). Moreover, [[HOXA5]] was previously found to promote the TGF-beta pathway. Interestingly, [[SMAD1]] is also a protein partner of the androgen receptor ([[AR]]) and an unsupervised analysis of gene ontology terms indicates that the [[AR]] pathway antagonizes the TGF-beta/SMAD pathway. Retrieval of promoter analysis data further confirmed that [[AR]] negatively regulates the transcription of several members of the TGF-beta/SMAD pathway. On this basis, we propose that in progressive MS patients, the physiological SC overexpression of [[HOXA5]] combined with the age-dependent decline in [[AR]] ligands may favor the slow progression of [[TGFB1]]-mediated gliosis. Potential therapeutic implications are discussed.
|mesh-terms=* Age Factors
* Aged
* Aging
* Brain
* Data Mining
* Databases, Genetic
* Disease Progression
* Female
* Gene Expression Profiling
* Gliosis
* Homeodomain Proteins
* Humans
* Ligands
* Male
* Middle Aged
* Multiple Sclerosis
* Proteomics
* Receptors, Androgen
* Sequence Analysis, RNA
* Signal Transduction
* Smad1 Protein
* Spinal Cord
* Transforming Growth Factor beta1
* Up-Regulation
|keywords=* androgen receptor
* astrocytes
* homeobox A5
* multiple sclerosis
* spinal cord
* transforming growth factor beta 1
|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6928867
}}
{{medline-entry
|title=Proteomic Alterations Associated with Biomechanical Dysfunction are Early Processes in the Emilin1 Deficient Mouse Model of Aortic Valve Disease.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/28812215
|abstract=Aortic valve (AV) disease involves stiffening of the AV cusp with progression characterized by inflammation, fibrosis, and calcification. Here, we examine the relationship between biomechanical valve function and proteomic changes before and after the development of AV pathology in the Emilin1-/- mouse model of latent AV disease. Biomechanical studies were performed to quantify tissue stiffness at the macro (micropipette) and micro (atomic force microscopy ([[AFM]])) levels. Micropipette studies showed that the Emilin1-/- AV annulus and cusp regions demonstrated increased stiffness only after the onset of AV disease. [[AFM]] studies showed that the Emilin1-/- cusp stiffens before the onset of AV disease and worsens with the onset of disease. Proteomes from AV cusps were investigated to identify protein functions, pathways, and interaction network alterations that occur with age- and genotype-related valve stiffening. Protein alterations due to Emilin1 deficiency, including changes in pathways and functions, preceded biomechanical aberrations, resulting in marked depletion of extracellular matrix (ECM) proteins interacting with [[TGFB1]], including latent transforming growth factor beta 3 (LTBP3), fibulin 5 (FBLN5), and cartilage intermediate layer protein 1 (CILP1). This study identifies proteomic dysregulation is associated with biomechanical dysfunction as early pathogenic processes in the Emilin1-/- model of AV disease.
|mesh-terms=* Animals
* Aortic Valve
* Bicuspid Aortic Valve Disease
* Biomechanical Phenomena
* Disease Models, Animal
* Extracellular Matrix Proteins
* Female
* Heart Defects, Congenital
* Heart Valve Diseases
* Male
* Membrane Glycoproteins
* Mice, Knockout
* Proteomics
* Transforming Growth Factor beta1
|keywords=* Aging
* Biomechanics
* Extracellular matrix
* Protein interaction networks
* Proteomics
* TGFbeta1
* Valves
|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5665708
}}
{{medline-entry
|title=Seminal plasma transforming growth factor-β, activin A and follistatin fluctuate within men over time.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/27609985
|abstract=Do seminal plasma transforming growth factor-β (TGFB) cytokines vary within individuals over time, and does this relate to sperm parameters, age or prior abstinence? Activin A and follistatin, and to a lesser extent [[TGFB1]], [[TGFB2]] and [[TGFB3]], vary within individuals over time, in association with duration of abstinence. Seminal plasma TGFB cytokines can influence sperm function and reproductive success through interactions with the female reproductive tract after coitus. Over time, individual sperm parameters fluctuate considerably. Whether seminal fluid TGFB cytokines vary similarly, and the determinants of any variance, is unknown. Between two and seven semen samples were collected from each of 14 fertile donors at 6-10 week intervals over the course of 12 months, then seminal plasma cytokines and sperm parameters were measured. The concentrations and total amounts per ejaculate of [[TGFB1]], [[TGFB2]], [[TGFB3]], activin A and follistatin were determined using commercial assays. Sperm parameters were assessed according to WHO IV standards. Mixed model analysis was utilised to determine the relative contribution of between- and within-individual factors to the variance. Relationships between cytokines and sperm parameters, as well as effect of age and duration of abstinence, were investigated by correlation analysis. Within-individual variability contributed to the total variance for all cytokines and sperm parameters, and was a stronger determinant than between-individual variability for activin A and follistatin as well as for total sperm concentration and sperm motility. Positive correlations between each of the three TGFB isoforms, and activin and follistatin, suggest co-regulation of synthesis. Duration of abstinence influenced total content of [[TGFB1]], [[TGFB2]], activin A and follistatin. [[TGFB1]] correlated inversely with age. A limited number of donors from a single clinic were investigated. Clinical information on BMI, nutrition, smoking and other lifestyle factors was unavailable. Further studies are required to determine whether the findings can be generalised to larger populations and different ethnicities. These data reveal substantial variation over time in seminal fluid cytokines and indicate that repeated analyses are required to gain precise representative data on an individual's status. Within-individual variation in seminal fluid components should be taken into account when investigating seminal fluid cytokines. This study was supported by grants from the National Health and Medical Research Council of Australia, ID453556 and APP1041332. The authors have no competing interests to disclose.
|mesh-terms=* Activins
* Adolescent
* Adult
* Age Factors
* Aging
* Follistatin
* Humans
* Male
* Middle Aged
* Semen
* Semen Analysis
* Sperm Count
* Transforming Growth Factor beta
* Young Adult
|keywords=* cytokines
* fertility
* seminal plasma
* sperm
* variation
|full-text-url=https://sci-hub.do/10.1093/humrep/dew185
}}
{{medline-entry
|title=No Association between Variation in Longevity Candidate Genes and Aging-related Phenotypes in Oldest-old Danes.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/26946122
|abstract=In this study we explored the association between aging-related phenotypes previously reported to predict survival in old age and variation in 77 genes from the DNA repair pathway, 32 genes from the growth hormone 1/ insulin-like growth factor 1/insulin (GH/IGF-1/INS) signalling pathway and 16 additional genes repeatedly considered as candidates for human longevity: [[APOE]], [[APOA4]], [[APOC3]], [[ACE]], [[CETP]], [[HFE]], [[IL6]], [[[[IL6]]R]], [[MTHFR]], [[TGFB1]], SIRTs 1, 3, 6; and HSPAs 1A, 1L, 14. Altogether, 1,049 single nucleotide polymorphisms (SNPs) were genotyped in 1,088 oldest-old (age 92-93 years) Danes and analysed with phenotype data on physical functioning (hand grip strength), cognitive functioning (mini mental state examination and a cognitive composite score), activity of daily living and self-rated health. Five SNPs showed association to one of the phenotypes; however, none of these SNPs were associated with a change in the relevant phenotype over time (7 years of follow-up) and none of the SNPs could be confirmed in a replication sample of 1,281 oldest-old Danes (age 94-100). Hence, our study does not support association between common variation in the investigated longevity candidate genes and aging-related phenotypes consistently shown to predict survival. It is possible that larger sample sizes are needed to robustly reveal associations with small effect sizes. 
|mesh-terms=* Activities of Daily Living
* Aged, 80 and over
* Aging
* Cognition
* Denmark
* Female
* Genotype
* Hand Strength
* Humans
* Linear Models
* Longevity
* Male
* Phenotype
* Polymorphism, Single Nucleotide
* Signal Transduction
* Surveys and Questionnaires
|keywords=* Association study
* Human aging
* Oldest-old
* Single nucleotide polymorphisms
|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4841709
}}