Effects of different cryoprotectants on the cryopreservation of cattle testicular tissue

Huang, Shan; Zhu, Qing-Chao; Han, Cong; Zhang, X.-G.; Song, B. Y.; Xie, Dixiang; Sang, Wei; Hu, Jianhong

doi:10.5194/aab-58-433-2015

Cited by 6 publications

(5 citation statements)

References 30 publications

(42 reference statements)

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“…MDA as a serum metabolic indicator can indirectly reflect the severity of myocardial cell injury . SOD is the main antioxidant enzyme in the body, which protects cells from free radical damage by scavenging oxygen free radicals . Therefore, it can be seen that in IRI mice, cardiomyocytes are damaged by oxygen free radicals, and OS is also enhanced.…”

Section: Discussionmentioning

confidence: 99%

“…28 SOD is the main antioxidant enzyme in the body, which protects cells from free radical damage by scavenging oxygen free radicals. 29 Therefore, it can be seen that in IRI mice, cardiomyocytes are damaged by oxygen free radicals, and OS is also enhanced. Our results also demonstrated that the overexpressed miR-590-3p and silenced RIPK1 showed increased Bcl-2 expression, and decreased expression of RIPK1, NF-κB, TLR4, caspase-3, FasL, p53, and cmyc.…”

Section: Downregulated Ripk1 Prolonged Cell Cycle Distribution and In...mentioning

confidence: 99%

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Retracted: Overexpression of microRNA‐590‐3p promotes the proliferation of and inhibits the apoptosis of myocardial cells through inhibition of the NF‐κB signaling pathway by binding to RIPK1

Zhao

Jiang

Wang

et al. 2018

J of Cellular Biochemistry

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Ischemic heart disease is widely considered as a major health threat, which causes a high number of deaths every year worldwide. Much evidence has shown that oxidative stress (OS) is implicated in the pathogenesis of ischemiareperfusion injury (IRI). This study aims to evaluate the effect of miR-590-3p on the OS of IRI mice through the nuclear factor kappa-B (NF-κB) signaling pathway by targeting receptor-interacting protein kinase 1 (RIPK1). IRI mouse models were established for extracting myocardial tissues and isolating myocardial cells. The expression of inflammatory related-factors was detected by enzyme-linked immunosorbent assay, and superoxide dismutase (SOD) and malondialdehyde (MDA) in tissues were determined. Reverse transcription quantitative polymerase chain reaction and Western blot analysis were performed to assess the role of miR-590-3p in the expression of NF-κB-related factors and apoptosis-related factors. Besides, the regulatory effects of miR-590-3p on myocardial cell proliferation and apoptosis were also assessed. According to the obtained results, we found that IRI mice displayed higher expression of tumor necrosis factor-α, interleukin (IL)-6, and interferon-γ, lower expression of IL-10 in serum, a decreased SOD level, and an increased MDA level. In addition, RIPK1 was determined as a target gene of miR-590-3p. After transfection of overexpressed miR-590-3p or si-RIPK1, declined RIPK1, NF-κB, Toll-like receptor 4, caspase-3, FasL, p53, and c-myc levels, increased B-cell lymphoma-2 level, promoted cell proliferation, promoted cell cycle distribution and inhibited apoptosis of myocardial cells were found. Our study demonstrates that miR-590-3p can alleviate the OS of IRI mice through the inhibition of the RIPK1 and NF-κB signaling pathway. Thus, miR-590-3p represents a potential target for IRI repair. K E Y W O R D S microRNA-590-3p, myocardial ischemia/reperfusion injury, nuclear factor kappa-B (NF-κB), oxidative stress (OS), receptor-interacting protein kinase 1 (RIPK1) J Cell Biochem. 2019;120:3559-3573.wileyonlinelibrary.com/journal/jcb Overexpression of microRNA-590-3p promotes the proliferation of and inhibits the apoptosis of myocardial cells through inhibition of the NF-κB signaling pathway by binding to RIPK1.

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Section: Discussionmentioning

confidence: 99%

Section: Downregulated Ripk1 Prolonged Cell Cycle Distribution and In...mentioning

confidence: 99%

Retracted: Overexpression of microRNA‐590‐3p promotes the proliferation of and inhibits the apoptosis of myocardial cells through inhibition of the NF‐κB signaling pathway by binding to RIPK1

Zhao

Jiang

Wang

et al. 2018

J of Cellular Biochemistry

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“…Cell viability depends on the thawing method, duration of cold storage, and reagents used (33). Relatively short storage periods (34) and optimal concentration of DMSO (10%) are crucial factors contributing to high cell viability in cryopreserved condition (32,(34)(35)(36). Other conditions not mentioned here may have an impact on the high cell viability in this study.…”

Section: Discussionmentioning

confidence: 82%

Regeneration of a Full-Thickness Defect of Rotator Cuff Tendon with Freshly Thawed Umbilical Cord-Derived Mesenchymal Stem Cells in a Rat Model

Yea

Park

Kim

et al. 2020

Preprint

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Background: It is difficult to immediately use mesenchymal stem cells (MSCs) for the patient with rotator cuff disease because isolation and culture time are required. Thus, the MSCs would be prepared in advanced in cryopreserved condition for an “off-the-shelf” usage in clinic. This study investigated the efficacy of freshly thawed MSCs on the regeneration of a full-thickness tendon defect (FTD) of rotator cuff tendon in a rat model. Methods: We evaluated morphology, viability and proliferation of cultured umbilical cord-derived MSCs (C-UC MSCs) and freshly thawed umbilical cord-derived MSCs (T-UC MSCs) at passage 10 in vitro. In animal experiments, we created a FTD in the supraspinatus tendon of rats and injected the injured tendon with saline, cryopreserved agent (CPA; control), C-UC MSCs, and T-UC MSCs respectively. Two to four weeks later, macroscopic, histological and biomechanical changes were evaluated. T-test and ANOVA were used with SPSS. Differences with p < .05 were considered statistically significant.Results: T-UC MSCs had fibroblast-like morphology and showed greater than 97% viability and stable proliferation comparable to the C-UC MSCs at passage 10. In animal experiments, compared with the control group, the macroscopic appearance of the T-UC MSCs was further recovered at two and four weeks such as inflammation, defect size, neighboring tendon, swelling/redness and the connecting surrounding tissue and slidability. Histologically, compared to the control group the nuclear aspect ratio, orientation angle of fibroblasts, collagen organization and fiber coherence were improved by 33.33%, 42.75%, 1.86- and 1.99-fold and GAG-rich area was suppressed by 81.05% at four weeks. Further, the T-UC MSCs showed enhanced ultimate failure load by 1.55- and 1.25-fold compared with the control group at both two and four weeks. All the improved values of T-UC MSCs were comparable to those of C-UC MSCs. Conclusions: The morphology, viability and proliferation of T-UC MSCs are comparable to those of C-UC MSCs. Treatment with T-UC MSCs induces tendon regeneration of FTD at the macroscopic, histological and biomechanical levels comparable to treatment with C-UC MSCs.

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“…Cell viability depends on the thawing method, duration of cold storage, and reagents used [36]. Relatively short storage periods [37] and optimal concentration of DMSO (10%) are crucial factors contributing to high cell viability in cryopreserved conditions [35,[37][38][39]. Other conditions not mentioned here may have an impact on the high cell viability in this study.…”

Section: Discussionmentioning

confidence: 82%

Regeneration of a full-thickness defect of rotator cuff tendon with freshly thawed umbilical cord-derived mesenchymal stem cells in a rat model

et al. 2020

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Background It is difficult to immediately use mesenchymal stem cells (MSCs) for the patient with rotator cuff disease because isolation and culture time are required. Thus, the MSCs would be prepared in advanced in cryopreserved condition for an “off-the-shelf” usage in clinic. This study investigated the efficacy of freshly thawed MSCs on the regeneration of a full-thickness tendon defect (FTD) of rotator cuff tendon in a rat model. Methods We evaluated morphology, viability, and proliferation of cultured umbilical cord-derived MSCs (C-UC MSCs) and freshly thawed umbilical cord-derived MSCs (T-UC MSCs) at passage 10 in vitro. In animal experiments, we created a FTD in the supraspinatus of rats and injected the injured tendon with saline, cryopreserved agent (CPA; control), C-UC MSCs, and T-UC MSCs, respectively. Two and 4 weeks later, macroscopic, histological, biomechanical, and cell trafficking were evaluated. T test and ANOVA were used with SPSS. Differences with p < .05 were considered statistically significant. Results T-UC MSCs had fibroblast-like morphology and showed greater than 97% viability and stable proliferation comparable to the C-UC MSCs at passage 10. In animal experiments, compared with the control group, the macroscopic appearance of the T-UC MSCs was more recovered at 2 and 4 weeks such as inflammation, defect size, neighboring tendon, swelling/redness, the connecting surrounding tissue and slidability. Histologically, the nuclear aspect ratio, orientation angle of fibroblasts, collagen organization, and fiber coherence were improved by 33.33%, 42.75%, 1.86-fold, and 1.99-fold at 4 weeks, and GAG-rich area decreased by 88.13% and 94.70% at 2 and 4 weeks respectively. Further, the T-UC MSCs showed enhanced ultimate failure load by 1.55- and 1.25-fold compared with the control group at both 2 and 4 weeks. All the improved values of T-UC MSCs were comparable to those of C-UC MSCs. Moreover, T-UC MSCs remained 8.77% at 4 weeks after injury, and there was no significant difference between C-UC MSCs and T-UC MSCs. Conclusions The morphology, viability, and proliferation of T-UC MSCs were comparable to those of C-UC MSCs. Treatment with T-UC MSCs could induce tendon regeneration of FTD at the macroscopic, histological, and biomechanical levels comparable to treatment with C-UC MSCs.

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Effects of different cryoprotectants on the cryopreservation of cattle testicular tissue

Cited by 6 publications

References 30 publications

Retracted: Overexpression of microRNA‐590‐3p promotes the proliferation of and inhibits the apoptosis of myocardial cells through inhibition of the NF‐κB signaling pathway by binding to RIPK1

Retracted: Overexpression of microRNA‐590‐3p promotes the proliferation of and inhibits the apoptosis of myocardial cells through inhibition of the NF‐κB signaling pathway by binding to RIPK1

Regeneration of a Full-Thickness Defect of Rotator Cuff Tendon with Freshly Thawed Umbilical Cord-Derived Mesenchymal Stem Cells in a Rat Model

Regeneration of a full-thickness defect of rotator cuff tendon with freshly thawed umbilical cord-derived mesenchymal stem cells in a rat model

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