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Objective: To investigate the expression and localization of Vasorin (Vasn) in human female reproductive system. Methods: The presence of Vasorin was evaluated by RT-PCR and immunoblotting analyses in patient-derived endometrial, myometrial and granulosa cells (GCs) primary cultures. Immunostaining analyses were performed to detect Vasn localization in primary cultures and in ovarian and uterine tissues. Results: Vasn mRNA was detected in patient-derived endometrial, myometrial and GCs primary cultures without significant differences at the transcript level. Otherwise, immunoblotting analysis showed that Vasn protein levels were significantly higher in GCs than proliferative endometrial stromal cells (ESCs) and myometrial cells. Immunohistochemistry performed in ovarian tissues revealed that Vasn was expressed in the GCs of ovarian follicles at different stages of development with a higher immunostaining signal in mature ovarian follicles such as the antral follicle or on the surface of cumulus oophorus cells than in early-stage follicles. The immunostaining of uterine tissues showed that Vasn was expressed in the proliferative stroma endometrium while it was significantly less expressed in the secretory endometrium. Conversely, no protein immunoreactivity was revealed in health myometrial tissue. Conclusions: Our results revealed the presence of Vasn in the ovary and the endometrium. The pattern of Vasn expression and distribution suggests that this protein may have a role in the regulation of processes such as folliculogenesis, oocyte maturation, and endometrial proliferation. [ABSTRACT FROM AUTHOR]

Sma and Mad related (SMAD)-mediated Transforming Growth Factor β (TGF-β) and Bone Morphogenetic Protein (BMP) signaling is required for various cellular processes. The activated heterotrimeric SMAD protein complexes associate with nuclear proteins such as the histone acetyltransferases p300, PCAF and the Mixed Lineage Leukemia 4 (MLL4) subunit Pax Transactivation domain-Interacting Protein (PTIP) to regulate gene transcription. We investigated the functional role of PTIP and PTIP Interacting protein 1 (PA1) in relation to TGF-β-activated SMAD signaling. We immunoprecipitated PTIP and PA1 with all SMAD family members to identify the TGF-β and not BMP-specific SMADs as interacting proteins. Gene silencing experiments of MLL4 and the subunits PA1 and PTIP confirm TGF-β-specific genes to be regulated by the MLL4 complex, which links TGF-β signaling to transcription regulation by the MLL4 methyltransferase complex. [ABSTRACT FROM AUTHOR]

Objectives: The objective of this review was to assess the literature for evidence investigating the role of TGF-β in temporomandibular joint disease with osteoarthritis.Method: An electronic and manual search was carried out on the databases, MEDLINE/PubMed, Cochrane Library, Web Of Science, and EMBASE, from 1975 to December 2015 by two independent evaluators to identify clinical and laboratory trials in English.Results: The search produced 693 records. Following a process of selection based on certain criteria, eight articles were included.Discussion: This systematic review suggests that TGF-β administration alone does not result in joint regeneration; other factors may be involved, such as TGF-β receptor expression ,and TGF-β receptor mutations that do not allow a correct transduction, resulting in TGF-β deficiency. The anabolism induced by this growth factor is also able to neutralize the catabolic processes that are elevated in osteoarthritis. Therefore, further studies are essential to determine how the concentration of TGF-β in the temporomandibular joints acts as a potential marker for the development of degenerative conditions. [ABSTRACT FROM AUTHOR]

This study aimed to investigate the synergy between transforming growth factor beta 3 (TGF-β3) and insulin-like growth factor 1 (IGF-1) on nucleus pulposus-derived mesenchymal stem cells (NP-MSCs) and the underlying mechanism using a serum-free culture system. NP-MSC proliferation and viability were measured using a CCK-8 assay and annexin V-FITC/propidium iodide, respectively. NP-MSCs in micromasses were investigated for differentiation towards nucleus pulposus cells (NPCs). SOX-9, collagen-I, collagen-II, aggrecan and decorin expressions were detected by RT-PCR and immunoblotting. Matrix deposition was assessed by sulfated glycosaminoglycan (sGAG) analysis. Novel chondrogenic and nucleus pulposus (NP) genes were detected to distinguish differentiated cell types. MAPK/ERK and TGF/Smad signaling pathways were also examined. As a result, the synergy between TGF-β3 and IGF-1 enhanced NP-MSC viability, extracellular matrix (ECM) biosynthesis and differentiation towards NPCs, partly through the activation of the MAPK/ERK signaling pathway. Therefore, the synergy between TGF-β3 and IGF-1 ameliorates NP-MSC viability, differentiation and promotes intervertebral disc regeneration. [ABSTRACT FROM AUTHOR]

PURPOSE. To determine if TGF-β regulates the expression of metalloproteinases in chick lens annular pad cells. METHODS. The activity of secreted matrix metalloproteinases was examined with gelatin zymography in primary cultures exposed to TGF-β. RESULTS. Metalloproteinases with electrophoretic mobilities corresponding to MMP2 and MMP9 were tentatively identified. Activated, processed forms of the two metalloproteinases were also observed. Plasminogen activators potentially capable of initiating metalloproteinase cascades were concomitantly elicited. Metalloproteinase secretion was shown to be specific for TGF-β stimulation and independent of substrate composition. CONCLUSIONS. These results indicate that TGF-β-mediated processes could be responsible for localized lens capsular heterogeneity, establishing a substrate suitable for cell migration or the release of matrix-bound factors which influence the terminal differentiation of lens cells. [ABSTRACT FROM AUTHOR]