Taurine is an effective therapy against thiram induced tibial dyschondroplasia via HIF-1α/VEGFA and β-catenin/ GSK-3β pathways in broilers

Ding, Yanmei; Yao, Wangyuan; Kulyar, Muhammad Fakhar‐e‐Alam; Mo, Quan; Pan, Huachun; Zhang, Yan; Ma, Bingjie; He, Ya; Zhang, Mengdi; Hong, Jiajia; Waqas, Muhammad; Li, Jiakui

doi:10.1016/j.ecoenv.2021.112981

Cited by 12 publications

(4 citation statements)

References 64 publications

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“…While the precise mechanism by which angiostatin suppresses angiogenesis remains unknown, this protein may cause endothelial cells to undergo apoptosis, preventing their proliferation and migration [84,112]. Similar increased apoptosis and inhibited proliferation occur in TD [52]. The suppression of MMP-mediated endothelial cell migration has also been suggested as the principal anti-angiogenic mechanism of angiostatin [113].…”

Section: Angiostatinmentioning

confidence: 99%

“…Experimental exposure to thiram causes downregulation of HIF-1α, VEGFA, VEGFR, and β-catenin expressions and upregulation of GSK-3β expression [52,53]. VEGF produced by hypertrophic chondrocytes [54], and regulated by HIF-1α [55].…”

Section: Hif-1α/vegf/vegfr Signaling Pathways Under Thiram Exposurementioning

confidence: 99%

“…VEGFR-1 reduces VEGFR-2 activity by appropriating and trapping VEGF, which prevents VEGFR-2 from binding to VEGF [126,127]. There is an increase in VEGF-A in TD but no corresponding rise in vasculature [52], which may be due to decoy receptors but requires some investigation.…”

Section: Decoy Receptorsmentioning

confidence: 99%

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Homeostatic Regulation of Pro-Angiogenic and Anti-Angiogenic Proteins via Hedgehog, Notch Grid, and Ephrin Signaling in Tibial Dyschondroplasia

Nawaz,

Kulyar,

et al. 2023

Animals

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Precise coupling of two fundamental mechanisms, chondrogenesis and osteogenesis via angiogenesis, plays a crucial role during rapid proliferation of growth plates, and alteration in their balance might lead to pathogenic conditions. Tibial dyschondroplasia (TD) is characterized by an avascular, non-mineralized, jade-white “cartilaginous wedge” with impaired endochondral ossification and chondrocyte proliferation at the proximal end of a tibial bone in rapidly growing poultry birds. Developing vascular structures are dynamic with cartilage growth and are regulated through homeostatic balance among pro and anti-angiogenic proteins and cytokines. Pro-angiogenic factors involves a wide spectrum of multifactorial mitogens, such as vascular endothelial growth factors (VEGF), platelet-derived growth factors (PDGF), basic fibroblast growth factor (bFGF), placental growth factors, transforming growth factor-β (TGF-β), and TNF-α. Considering their regulatory role via the sonic hedgehog, notch-gridlock, and ephrin-B2/EphB4 pathways and inhibition through anti-angiogenic proteins like angiostatin, endostatin, decoy receptors, vasoinhibin, thrombospondin, PEX, and troponin, their possible role in persisting inflammatory conditions like TD was studied in the current literature review. Balanced apoptosis and angiogenesis are vital for physiological bone growth. Any homeostatic imbalance among apoptotic, angiogenetic, pro-angiogenic, or anti-angiogenic proteins ultimately leads to pathological bone conditions like TD and osteoarthritis. The current review might substantiate solid grounds for developing innovative therapeutics for diseases governed by the disproportion of angiogenesis and anti-angiogenesis proteins.

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Section: Angiostatinmentioning

confidence: 99%

Section: Hif-1α/vegf/vegfr Signaling Pathways Under Thiram Exposurementioning

confidence: 99%

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Homeostatic Regulation of Pro-Angiogenic and Anti-Angiogenic Proteins via Hedgehog, Notch Grid, and Ephrin Signaling in Tibial Dyschondroplasia

Nawaz,

Kulyar,

et al. 2023

Animals

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“…The pathogenesis of TD is complex and diverse, but the uncontrolled growth, differentiation, and apoptosis of growth plate chondrocytes are recognized as the primary evidence [ 2 , 3 , 4 ]. Although significant coupling between the regulation of chondrocyte growth, terminal differentiation, and the recruitment of growth plate blood vessels has been demonstrated [ 5 , 6 , 7 ], the mechanisms underlying precise the coordination of proliferation, differentiation, formation, and the invasion of blood vessels remain unknown in the growth plate [ 8 , 9 ].…”

Section: Introductionmentioning

confidence: 99%

The Effect of miR-140-5p with HDAC4 towards Growth and Differentiation Signaling of Chondrocytes in Thiram-Induced Tibial Dyschondroplasia

Yao,

Kulyar,

Ding

et al. 2023

IJMS

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There is evidence to suggest that microRNA-140-5p (miR-140), which acts as a suppressor, is often elevated and has a role in various malignancies. Nevertheless, neither the function nor the mechanisms in chondrocytes linked with bone disorders, e.g., tibial dyschondroplasia (TD), have been satisfactorily established. The purpose of this study was to look into the role of microRNA-140-5p (miR-140) and its interaction with HDAC4 in chondrocytes, as well as the implications for tibial dyschondroplasia (TD), with a particular focus on the relationship between low miR-140 expression and poor pathologic characteristics, as well as its physiological effects on chondrocyte growth, differentiation, and chondrodysplasia. In this investigation, we discovered that TD had a reduced expression level of the miR-140. There was a correlation between low miR-140 expression, poor pathologic characteristics, and the short overall survival of chondrocytes. Our findings show an aberrant reduction in miR-140 expression, and HDAC4 overexpression caused disengagement in resting and proliferation zones. This further resulted in uncontrolled cell proliferation, differentiation, and chondrodysplasia. Mechanistically, HDAC4 inhibited the downstream transcription factors MEF2C and Runx2 and interacted with Col-Ⅱ, Col-X, and COMP. However, miR-140 binding to the 3′-UTR of HDAC4 resulted in the growth and differentiation of chondrocytes. Moreover, the expression of HDAC4 through LMK-235 was significantly decreased, and the expression was significantly increased under ITSA-1, referring to a positive feedback circuit of miR-140 and HDAC4 for endochondral bone ossification. Furthermore, as a prospective treatment, the flavonoids of Rhizoma drynariae (TFRD) therapy increased the expression of miR-140. Compared to the TD group, TFRD treatment increased the expression of growth-promoting and chondrocyte differentiation markers, implying that TFRD can promote chondrocyte proliferation and differentiation in the tibial growth plate. Hence, directing this circuit may represent a promising target for chondrocyte-related bone disorders and all associated pathological bone conditions.

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Molecular mechanisms of environmental pollutant-induced cartilage damage: from developmental disorders to osteoarthritis

Skalny,

Aschner,

Zhang

et al. 2024

Arch Toxicol

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Taurine is an effective therapy against thiram induced tibial dyschondroplasia via HIF-1α/VEGFA and β-catenin/ GSK-3β pathways in broilers

Cited by 12 publications

References 64 publications

Homeostatic Regulation of Pro-Angiogenic and Anti-Angiogenic Proteins via Hedgehog, Notch Grid, and Ephrin Signaling in Tibial Dyschondroplasia

Homeostatic Regulation of Pro-Angiogenic and Anti-Angiogenic Proteins via Hedgehog, Notch Grid, and Ephrin Signaling in Tibial Dyschondroplasia

The Effect of miR-140-5p with HDAC4 towards Growth and Differentiation Signaling of Chondrocytes in Thiram-Induced Tibial Dyschondroplasia

Molecular mechanisms of environmental pollutant-induced cartilage damage: from developmental disorders to osteoarthritis

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