Altered Chondrocyte Apoptosis Status in Developmental Hip Dysplasia in Rabbits

Yi, Wei; Li, Dai He; Liu, Wan Lin; Jiang, Dian Ming

doi:10.5152/balkanmedj.2016.150557

Cited by 13 publications

(16 citation statements)

References 24 publications

(18 reference statements)

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“…7 And our results showed that WISP-2 was remarkedly upregulated in hip cartilage of DDH rats. According to our results, WISP-2 may be involved in chondrocyte apoptosis that is important for both DDH and osteoarthritis, 3,33,40,41 possibly through similar mechanisms. However, the etiology of DDH and osteoarthritis are both complicated and not yet fully understood, thus we are not sure whether our DDH model can represent the pathological process of osteoarthritis.…”

Section: Discussionsupporting

confidence: 60%

“…[14][15][16][17] Since straight-leg swaddling had been demonstrated as an exact contributing factor for DDH, researchers started to fix the hind legs and/ or hip joint of rats and rabbits in hip adduction and knee extension to establish DDH models. 3,18,19 In this study, we observed the cartilage apoptosis in both the acetabulum and proximal femoral epiphysis and measured the expressions of WISP-2 and PPARγ in a rat DDH model. Then we further investigated whether WISP-2 may function as a pro-apoptotic role in chondrocytes through PPARγ by gene knockdown or knockin of WISP-2 and PPARγ in primary chondrocytes in vitro.…”

Section: Introductionmentioning

confidence: 99%

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WISP‐2, an upregulated gene in hip cartilage from the DDH model rats, induces chondrocyte apoptosis through PPARγ in vitro

Liu

Zhao

et al. 2020

The FASEB Journal

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Chondrocyte apoptosis plays an important role in the developmental dysplasia of the hip (DDH) development. It has been found that WNT1 inducible signaling pathway protein 2 (WISP‐2) and peroxisome proliferator‐activated receptor γ (PPARγ) are involved in cell apoptosis. In this study, we performed the straight‐leg swaddling DDH rat model and we found that cartilage degradation and chondrocyte apoptosis were remarkably increased in DDH rats in vivo. Moreover, we found that WISP‐2 was upregulated in hip acetabular cartilage of DDH rats compared to control rats. Next, the effects of WISP‐2 on chondrocyte apoptosis and its possible underlying mechanism were examined in vitro. The lentivirus‐mediated gain‐ and loss‐of‐function experiments of WISP‐2 and peroxisome proliferator‐activated receptor γ (PPARγ) for cell viability and apoptosis were performed in primary rat chondrocytes. The results showed that the overexpression of WISP‐2 induced chondrocyte apoptosis, and knockdown of WISP‐2 could suppress the chondrocyte apoptosis induced by advanced glycation end products (AGE). Additionally, WISP‐2 could negatively regulate the expression of PPARγ in chondrocytes. Moreover, the knockdown of PPARγ promoted chondrocyte apoptosis and overexpression of PPARγ abated the increased apoptosis and decreased cell viability of chondrocytes induced by WISP‐2. This study demonstrated that WISP‐2 might contribute to chondrocyte apoptosis of hip acetabular cartilage through regulating PPARγ expression and activation, which may play an important role in the development of DDH.

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Section: Discussionsupporting

confidence: 60%

Section: Introductionmentioning

confidence: 99%

WISP‐2, an upregulated gene in hip cartilage from the DDH model rats, induces chondrocyte apoptosis through PPARγ in vitro

Liu

Zhao

et al. 2020

The FASEB Journal

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“…Increasing amounts of evidence has shown that chondrocyte apoptosis have great roles in cartilage development, aging and disease. 24 NO has emerged as a key factor for mediation of chondrocyte apoptosis in OA. 25 It has been suggested that either endogenous or exogenous NO can induce apoptosis in chondrocytes via a mitochondria-dependent mechanism.…”

Section: Discussionmentioning

confidence: 99%

Increased 15-lipoxygenase-1 expression in chondrocytes contributes to the pathogenesis of osteoarthritis

Chen

Yan

et al. 2017

Cell Death Dis

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15-Lipoxygenase-1 (15-LO-1) is involved in many pathological processes. The purpose of this study was to determine the potential role of 15-LO-1 in osteoarthritis (OA). The levels of 15-LO-1 expression were measured by western blotting and quantitative real-time PCR in articular cartilage from the OA rat models and OA patients. To further investigate the effects of 15-LO-1 on chondrocyte functions, such as extracellular matrix (ECM) secretion, the release of matrix-degrading enzymes, the production of reactive oxygen species (ROS), cell proliferation and apoptosis, we decreased or increased 15-LO-1 expression in chondrocytes by means of transfecting with siRNA targeting 15-LO-1 and plasmid encoding 15-LO-1, respectively. The results showed that 15-LO-1 expression was obviously increased in articular cartilage from OA rats and OA patients. It was also found that many factor-related OA, such as mechanical loading, ROS, SNP and inflammatory factor, significantly promoted 15-LO-1 expression and activity in chondrocytes. Silencing 15-LO-1 was able to markedly alleviate mechanical loading-induced cartilage ECM secretion, cartilage-degrading enzyme secretion and ROS production. Overexpression of 15-LO-1 could inhibit chondrocyte proliferation and induce chondrocyte apoptosis. In addition, reduction of 15-LO-1 in vivo significantly alleviated OA. Taken together, these results indicate that 15-LO-1 has an important role in the disease progression of OA. Thus 15-LO-1 may be a good target for developing drugs in the treatment of OA.

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“…The PI3K/Akt pathway, a vital anti-apoptotic pathway in cells, can suppress apoptosis by regulating the death receptor pathway and the mitochondrial pathway [14]. The PI3K/Akt pathway can regulate the expression of many anti-apoptotic genes by its downstream transcription factor [15]. As a major downstream target of PI3K, Akt can phosphorylate multiple proteins to regulate cell survival [16,17].…”

Section: Introductionmentioning

confidence: 99%

Over-Expression of ATPase II Alleviates Ethanol-Induced Hepatocyte Injury in HL-7702 Cells

Yang

Liu

2018

Med Sci Monit

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BackgroundExcessive alcohol consumption can cause hepatocellular injury. ATPase II (ATP8A1) can display an ATP-dependent phospholipid translocase activity. However, the function of ATP8A1 in hepatocyte injury is still unclear. In the present study we explored the effect of ATP8A1 on ethanol-induced hepatocyte injury.Material/MethodA human hepatocyte strain, HL-7702, was pretreated by ethanol with gradient concentration for 2, 4, 8, and 12 h, and were then divided into 6 groups after the cells were transfected. We detected cell viability by use of the Cell Counting Kit-8 (CCK-8) assay. Reactive oxygen species (ROS), apoptosis rate, and mitochondrial membrane potential (MMP) were measured using flow cytometry. We used quantitative reverse transcription-polymerase chain reaction (qRT-PCR) and Western blot to measure the mRNA and protein expression, respectively.ResultsEthanol inhibited the viability of HL-7702 cells and suppressed the expression of ATP8A1 in dose- and time-dependent manners. Furthermore, over-expression of ATP8A1 reduced the level of ROS and the apoptosis rate and recovered the MMP. Additionally, over-expressed ATP8A1 regulated the protein and mRNA levels of apoptosis-related molecules. Moreover, over-expression of ATP8A1 enhanced the phosphorylation of phosphatidylinositol 3-kinase (PI3K) and protein kinase B (Akt).ConclusionsOver-expression of ATP8A1 alleviated ethanol-induced hepatocyte injury. Moreover, the PI3K/Akt signaling pathway appears to participate in inhibition of ethanol-induced hepatocyte apoptosis and may provide a candidate target for the treatment of alcoholic liver diseases (ALD).

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Altered Chondrocyte Apoptosis Status in Developmental Hip Dysplasia in Rabbits

Cited by 13 publications

References 24 publications

WISP‐2, an upregulated gene in hip cartilage from the DDH model rats, induces chondrocyte apoptosis through PPARγ in vitro

WISP‐2, an upregulated gene in hip cartilage from the DDH model rats, induces chondrocyte apoptosis through PPARγ in vitro

Increased 15-lipoxygenase-1 expression in chondrocytes contributes to the pathogenesis of osteoarthritis

Over-Expression of ATPase II Alleviates Ethanol-Induced Hepatocyte Injury in HL-7702 Cells

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