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المؤلفون: Jun Ge, Cenhao Wu, Feng Zhou, Qi Yan, Huilin Yang, Xiaoqiang Cheng, Jun Zou, Yingjie Wang, Hao Yu
المصدر: Journal of Cellular and Molecular Medicine
مصطلحات موضوعية: 0301 basic medicine, Calcitonin, Male, Nucleus Pulposus, Biopsy, Cell, Interleukin-1beta, Matrix (biology), 03 medical and health sciences, 0302 clinical medicine, medicine, Animals, Protein kinase C, Cells, Cultured, Protein Kinase C, intervertebral disc degeneration, Chemistry, Intervertebral disc, Cell Biology, Original Articles, Chondrogenesis, Immunohistochemistry, Cell biology, Rats, Blot, 030104 developmental biology, medicine.anatomical_structure, rat caudal model, 030220 oncology & carcinogenesis, Molecular Medicine, Phosphorylation, Original Article, Disease Susceptibility, Biomarkers, Signal Transduction
الوصف: Intervertebral disc degeneration (IVDD) is the most critical factor that causes low back pain. Molecular biotherapy is a fundamental strategy for IVDD treatment. Calcitonin can promote the proliferation of chondrocytes, stimulate the synthesis of matrix and prevent cartilage degeneration. However, its effect and the underlying mechanism for IVDD have not been fully revealed. Chondrogenic specific matrix components’ mRNA expression of nucleus pulposus cell (NPC) was determined by qPCR. Protein expression of NPC matrix components and protein kinase C was determined by Western blotting. A rat caudal intervertebral disc degeneration model was established and tested for calcitonin in vivo. IL‐1 induced NPC change via decreasing protein kinase C (PKC)‐ε phosphorylation, while increasing PKC‐δ phosphorylation. Calcitonin treatment could prevent or reverse IL‐1‐induced cellular change on PKC signalling associated with degeneration. The positive effect of calcitonin on IVDD in vivo was verified on a rat caudal model. In summary, this study, for the first time, elucidated the important role of calcitonin in the regulation of matrix components in the nucleus of the intervertebral disc. Calcitonin can delay degeneration of the intervertebral disc nucleus by activating the PKC‐ε pathway and inhibiting the PKC‐δ pathway.
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المؤلفون: Nan Du, Bingqiang He, Hui Li, Ting Yang, Chunshuai Sun, Honghua Song, Yongjun Wang, Yingjie Wang
المصدر: The Journal of Biological Chemistry
مصطلحات موضوعية: 0301 basic medicine, cell migration, eAS, embryonic rat astrocytes, IPTG, isopropyl-b-D-thiogalactopyranoside, Biochemistry, neuroinflammation, TLRs, Toll-like receptors, MIF, macrophage migration inhibitory factor, NODs, oligomerization domain proteins, Cell Movement, cytokine, GFAP, glial fibrillary acid protein, ANOVA, analysis of variance, Cells, Cultured, DAMPs, damage-associated molecular pattern molecules, immunosuppression, MIF, Cell migration, ELISA, enzyme-linked immunosorbent assay, gAS, adult gecko astrocytes, Neural stem cell, Cell biology, medicine.anatomical_structure, rAS, adult rat astrocytes, DMEM, Dulbecco's modified eagle's medium, medicine.symptom, Q-PCR, quantitative real-time polymerase chain reaction, Inflammation Mediators, Astrocyte, Research Article, Central nervous system, PBS, phosphate-buffered saline, Inflammation, Biology, Proinflammatory cytokine, 03 medical and health sciences, SCI, spinal cord injury, astrocyte, IPA, Ingenuity Pathway Analysis Software, medicine, Animals, Proto-Oncogene Proteins c-vav, Molecular Biology, Macrophage Migration-Inhibitory Factors, Neuroinflammation, Cell Proliferation, 030102 biochemistry & molecular biology, spinal cord, Reptiles, Cell Biology, Rats, reptile, 030104 developmental biology, Vav1, Astrocytes, Macrophage migration inhibitory factor, NSC, neural stem cell, 4-IPP, 4-iodo-6-phenylpyrimidine, MAPK, mitogen-activated protein kinase, Biomarkers
الوصف: Adult mammalian astrocytes are sensitive to inflammatory stimuli in the context of neuropathology or mechanical injury, thereby affecting functional outcomes of the central nervous system (CNS). In contrast, glial cells residing in the spinal cord of regenerative vertebrates exhibit a weak astroglial reaction similar to those of mammals in embryonic stages. Macrophage migration inhibitory factor (MIF) participates in multiple neurological disorders by activation of glial and immune cells. However, the mechanism of astrocytes from regenerative species, such as gecko astrocytes (gAS), in resistance to MIF-mediated inflammation in the severed cords remains unclear. Here, we compared neural stem cell markers among gAS, as well as adult (rAS) and embryonic (eAS) rat astrocytes. We observed that gAS retained an immature phenotype resembling rat eAS. Proinflammatory activation of gAS with gecko (gMIF) or rat (rMIF) recombinant protein was unable to induce the production of inflammatory cytokines, despite its interaction with membrane CD74 receptor. Using cross-species screening of inflammation-related mediators from models of gMIF- and rMIF-induced gAS and rAS, we identified Vav1 as a key regulator in suppressing the inflammatory activation of gAS. The gAS with Vav1 deficiency displayed significantly restored sensitivity to inflammatory stimuli. Meanwhile, gMIF acts to promote the migration of gAS through regulation of CXCL8 following cord lesion. Taken together, our results suggest that Vav1 contributes to the regulation of astrocyte-mediated inflammation, which might be beneficial for the therapeutic development of neurological diseases.
URL الوصول: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::fbbceb6a544772110ebb1526ac88afb3
http://europepmc.org/articles/PMC8065226 -
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المؤلفون: Simon M. Sandford, Fernando Porcelli, Cristina Olivieri, V. S. Manu, David D. Thomas, Donald K. Blumenthal, Susan S. Taylor, Caitlin Walker, Yingjie Wang, Gianluigi Veglia, David A. Bernlohr, Adak Karamafrooz
المصدر: Communications Biology
Communications Biology, Vol 4, Iss 1, Pp 1-11 (2021)مصطلحات موضوعية: 0301 basic medicine, genetic structures, QH301-705.5, Kinase, Chemistry, Allosteric regulation, Medicine (miscellaneous), Cooperativity, Fusion protein, General Biochemistry, Genetics and Molecular Biology, Article, PRKACA, Cell biology, 03 medical and health sciences, 030104 developmental biology, 0302 clinical medicine, 030220 oncology & carcinogenesis, Heat shock protein, Phosphorylation, Biology (General), General Agricultural and Biological Sciences, Protein kinase A, Solution-state NMR
الوصف: An aberrant fusion of the DNAJB1 and PRKACA genes generates a chimeric protein kinase (PKA-CDNAJB1) in which the J-domain of the heat shock protein 40 is fused to the catalytic α subunit of cAMP-dependent protein kinase A (PKA-C). Deceivingly, this chimeric construct appears to be fully functional, as it phosphorylates canonical substrates, forms holoenzymes, responds to cAMP activation, and recognizes the endogenous inhibitor PKI. Nonetheless, PKA-CDNAJB1 has been recognized as the primary driver of fibrolamellar hepatocellular carcinoma and is implicated in other neoplasms for which the molecular mechanisms remain elusive. Here we determined the chimera’s allosteric response to nucleotide and pseudo-substrate binding. We found that the fusion of the dynamic J-domain to PKA-C disrupts the internal allosteric network, causing dramatic attenuation of the nucleotide/PKI binding cooperativity. Our findings suggest that the reduced allosteric cooperativity exhibited by PKA-CDNAJB1 alters specific recognitions and interactions between substrates and regulatory partners contributing to dysregulation.
Olivieri, Walker, Karamafrooz et al. show that the fusion of the dynamic J-domain to PKA-C (PKA-CDNAJB1) disrupts the internal allosteric network, attenuating the nucleotide/PKI binding cooperativity. This study suggests that the reduced allosteric cooperativity may contribute to the pathology that PKA-CDNAJB1 drives. -
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المؤلفون: Aisong Guo, Yuxin Zhang, Tiancheng Song, Yingjie Wang, Nan Du, Yongjun Wang, Zhenjie Zhu, Yue Zhou, Shuxia Chen, Yumin Yang, Yuming Hu
المصدر: Journal of Neuroinflammation, Vol 16, Iss 1, Pp 1-15 (2019)
Journal of Neuroinflammationمصطلحات موضوعية: 0301 basic medicine, MAPK/ERK pathway, Male, Indoles, CD74, lcsh:RC346-429, Rats, Sprague-Dawley, 0302 clinical medicine, Spinal cord injury, Cells, Cultured, Spinal cord, General Neuroscience, MIF, Cell biology, medicine.anatomical_structure, Neurology, PGE2, medicine.symptom, Astrocyte, COX2, Immunology, Inflammation, S100 Calcium Binding Protein beta Subunit, Biology, Dinoprostone, Proinflammatory cytokine, 03 medical and health sciences, Cellular and Molecular Neuroscience, Cell surface receptor, Glial Fibrillary Acidic Protein, medicine, Animals, Macrophage Migration-Inhibitory Factors, Spinal Cord Injuries, lcsh:Neurology. Diseases of the nervous system, Research, Macrophages, Histocompatibility Antigens Class II, medicine.disease, Rats, Antigens, Differentiation, B-Lymphocyte, Disease Models, Animal, 030104 developmental biology, Animals, Newborn, Prostaglandin-Endoperoxide Synthases, Astrocytes, Culture Media, Conditioned, Macrophage migration inhibitory factor, 030217 neurology & neurosurgery
الوصف: Background Astrocytes have been shown to produce several pro- and anti-inflammatory cytokines to maintain homeostasis of microenvironment in response to vast array of CNS insults. Some inflammation-related cytokines are responsible for regulating such cell events. Macrophage migration inhibitory factor (MIF) is a proinflammatory cytokine that can be inducibly expressed in the lesioned spinal cord. Unknown is whether MIF can facilitate the production of immunosuppressive factors from astrocytes to tune milieu following spinal cord injury. Methods Following establishment of contusion SCI rat model, correlation of PGE2 synthesis-related protein levels with that of MIF was assayed by Western blot. ELISA assay was used to detect production of PGE2, TNF-α, IL-1β, and IL-6. Immunohistochemistry was performed to observe colocalization of COX2 with GFAP- and S100β-positive astrocytes. The primary astrocytes were treated by various inhibitors to validate relevant signal pathway. Results The protein levels of MIF and COX2, but not of COX1, synchronously increased following spinal cord injury. Treatment of MIF inhibitor 4-IPP to the lesion sites significantly reduced the expression of COX2, mPGES-1, and as a consequence, the production of PGE2. Astrocytes responded robustly to the MIF interference, by which regulated MAPK/COX2/PGE2 signal pathway through coupling with the CD74 membrane receptor. MIF-induced production of PGE2 from astrocytes was able to suppress production of TNF-α, but boosted production of IL-1β and IL-6 in LPS-activated macrophages. Conclusion Collectively, these results reveal a novel function of MIF-mediated astrocytes, which fine-tune inflammatory microenvironment to maintain homeostasis. These suggest an alternative therapeutic strategy for CNS inflammation. Electronic supplementary material The online version of this article (10.1186/s12974-019-1468-6) contains supplementary material, which is available to authorized users.
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المؤلفون: Yingjie Wang, Manu V S, Jonggul Kim, Lalima G. Ahuja, Susan S. Taylor, Geoffrey Li, Philip Aoto, Gianluigi Veglia
المصدر: Nature Communications, Vol 10, Iss 1, Pp 1-11 (2019)
Nature Communicationsمصطلحات موضوعية: Models, Molecular, 0301 basic medicine, Protein Conformation, Entropy, Science, Allosteric regulation, General Physics and Astronomy, Cooperativity, 02 engineering and technology, Calorimetry, Molecular Dynamics Simulation, Article, General Biochemistry, Genetics and Molecular Biology, Enzyme catalysis, 03 medical and health sciences, Adenosine Triphosphate, Protein structure, Allosteric Regulation, Catalytic Domain, lcsh:Science, Protein kinase A, Nuclear Magnetic Resonance, Biomolecular, chemistry.chemical_classification, Multidisciplinary, Cooperative binding, General Chemistry, Conformational entropy, 021001 nanoscience & nanotechnology, Cyclic AMP-Dependent Protein Kinases, Adenosine Diphosphate, 030104 developmental biology, Enzyme, chemistry, Biophysics, lcsh:Q, 0210 nano-technology
الوصف: Enzymes accelerate the rate of chemical transformations by reducing the activation barriers of uncatalyzed reactions. For signaling enzymes, substrate recognition, binding, and product release are often rate-determining steps in which enthalpy-entropy compensation plays a crucial role. While the nature of enthalpic interactions can be inferred from structural data, the molecular origin and role of entropy in enzyme catalysis remains poorly understood. Using thermocalorimetry, NMR, and MD simulations, we studied the conformational landscape of the catalytic subunit of cAMP-dependent protein kinase A, a ubiquitous phosphoryl transferase involved in a myriad of cellular processes. Along the enzymatic cycle, the kinase exhibits positive and negative cooperativity for substrate and nucleotide binding and product release. We found that globally coordinated changes of conformational entropy activated by ligand binding, together with synchronous and asynchronous breathing motions of the enzyme, underlie allosteric cooperativity along the kinase’s cycle.
Allosteric interactions are an important contributor to the catalytic properties of enzyme. Here the authors demonstrate—using the prototypical protein kinase PKA—that the allosteric cooperativity underscoring substrate recognition and product release are directly linked to changes in conformational entropy. -
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المؤلفون: Wenjuan Wang, Yuming Hu, Yingjie Wang, Wei Guo, Zongyu Guan, Tiancheng Song, Yue Zhou, Xuejie Zhang, Zhenjie Zhu, Kaini Yang, Yongjun Wang, Nan Du, Aisong Guo
المصدر: Journal of Neuroinflammation, Vol 15, Iss 1, Pp 1-12 (2018)
Journal of Neuroinflammationمصطلحات موضوعية: Male, 0301 basic medicine, Chemokine, CD74, lcsh:RC346-429, Rats, Sprague-Dawley, 0302 clinical medicine, Cell Movement, RNA, Small Interfering, Chemokine CCL5, Spinal cord injury, Cells, Cultured, Spinal cord, Interleukin-13, biology, CCL5, Chemistry, General Neuroscience, MIF, Cell biology, Intramolecular Oxidoreductases, Intracellular signal transduction, medicine.anatomical_structure, Neurology, medicine.symptom, Chemokines, Astrocyte, MAP Kinase Signaling System, Immunology, Inflammation, Motor Activity, 03 medical and health sciences, Cellular and Molecular Neuroscience, Glial Fibrillary Acidic Protein, medicine, Animals, Macrophage Migration-Inhibitory Factors, Spinal Cord Injuries, lcsh:Neurology. Diseases of the nervous system, Research, Histocompatibility Antigens Class II, medicine.disease, Rats, Antigens, Differentiation, B-Lymphocyte, Disease Models, Animal, Pyrimidines, 030104 developmental biology, Animals, Newborn, Gene Expression Regulation, Astrocytes, biology.protein, Macrophage migration inhibitory factor, 030217 neurology & neurosurgery
الوصف: Background Astrocytes act as immune effector cells with the ability to produce a wide array of chemokines and cytokines in response to various stimuli. Macrophage migration inhibitory factor (MIF) is inducibly expressed in injured spinal cord contributing to excessive inflammation that affects motor functional recovery. Unknown is whether MIF can facilitate inflammatory responses through stimulating release of chemokines from astrocytes following spinal cord injury. Methods Following the establishment of the contusion spinal cord injury rat model, the correlation of chemokine (C-C motif) ligand 5 (CCL5) expression with that of MIF was assayed by Western blot, ELISA, and immunohistochemistry. Immunoprecipitation was used to detect MIF interaction with membrane CD74 receptor. Intracellular signal transduction of MIF/CD74 axis was analyzed by transcriptome sequencing of primary astrocytes and further validated by treatment of various inhibitors. The effects of CCL5 released by astrocytes on macrophage migration were performed by transwell migration assay. The post-injury locomotor functions were assessed using the Basso, Beattie, and Bresnahan (BBB) locomotor scale. Results The protein levels of chemokine CCL5/RANTES were remarkably increased in the astrocytes of rat injured spinal cord, in parallel with the expression of MIF. Treatment of MIF inhibitor 4-IPP in the lesion sites resulted in a significant decrease of CCL5 protein levels. In vitro study revealed MIF was capable of facilitating CCL5 production of astrocytes through interaction with CD74 membrane receptor, and knockdown of this receptor attenuated such effects. Production of CCL5 in astrocytes was significantly blocked by inhibitor of c-Jun N-terminal kinase, rather than by those of ERK and P38. Recombinant CCL5 protein was found to be more effective in promoting migration of M2- compared to M1-type macrophages. Conclusion Collectively, these data reveal a novel function of MIF in regulation of CCL5 release from astrocytes, which in turn favors for recruitment of inflammatory cells to the injured site of the spinal cord, in association with activation of excessive inflammation. Electronic supplementary material The online version of this article (10.1186/s12974-018-1297-z) contains supplementary material, which is available to authorized users.
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المؤلفون: Yi Li, Yani Zhang, Wenhui Zhang, Man Wang, Qisheng Zuo, Ahmed Elsayed, Cai Hu, Bichun Li, Yingjie Wang
المصدر: Stem Cells International
Stem Cells International, Vol 2021 (2021)مصطلحات موضوعية: 0301 basic medicine, Article Subject, Mechanism (biology), Wnt signaling pathway, Cell Biology, Biology, Embryonic stem cell, RC31-1245, Cell biology, 03 medical and health sciences, 030104 developmental biology, 0302 clinical medicine, 030220 oncology & carcinogenesis, Reproductive process, microRNA, Target gene, Stem cell, Molecular Biology, Internal medicine, Research Article
الوصف: MicroRNAs (miRNAs) are essential factors in the reproductive process of poultry. Here, we found miR-302d is a potential differentiation and negative factor of chicken embryonic stem cells (ESCs) into spermatogonia stem cells (SSCs). The competition mechanism was carried out for the preliminary exploration to determine the relationship among miR-302d, lncRNA-341(interacting with miR-302d), and target gene TLE4. The results showed that lncRNA-341 can competitively bind to miR-302d to decrease the targeted binding of miR-302d and TLE4 which promotes the differentiation of chicken SSCs. Moreover, it is suggested that miR-302d may participate in the Wnt signaling pathway through TLE4.
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المؤلفون: Kai Jin, Yan-qing Ji, Shaoze Cheng, Qisheng Zuo, Na-na He, Chen Zhang, Yani Zhang, Wen-ming Zhao, Xin-jian Yu, Li Bichun, Yilin Wang, Yingjie Wang, Fei Wang, Zhen-yu Lu, Dong Li, Ruifeng Zhao, Man Wang
المصدر: Journal of Integrative Agriculture, Vol 16, Iss 10, Pp 2257-2263 (2017)
مصطلحات موضوعية: 0301 basic medicine, animal structures, Agriculture (General), Plant Science, Biology, Biochemistry, dosage, chicken embryos injection, S1-972, Andrology, Toxicology, chick embryo development, 03 medical and health sciences, Food Animals, Injection site, Eggshell, Ecology, Experimental model, Hatching, Embryogenesis, Embryo, Trypan blue stain, 030104 developmental biology, embryonic structures, Animal Science and Zoology, hatchability, Agronomy and Crop Science, Food Science
الوصف: In biological research, chicken embryos are a classic experimental model for the exploration of the embryonic development and cell differentiation. Transferring exogenous substances into chicken embryos for producing medical antibodies has been widely used in the production practice. However, there are few studies about the effect of the different injection site and dosage on chicken embryos. The aim of this study was to explore the effects of different injection sites and dosages on chicken embryo hatching rate and development, so as to provide a basis for further studies using the chicken embryo model. Freshly laid eggs (Rugao yellow chicken) were injected with different doses of saline at the tip, equatorial plane and the blunt end of the egg shell, respectively. Egg hatching rate was recorded and compared among injection sites and different doses. A trypan blue stain was also injected at the aforementioned sites and the growth of chicken embryos was observed. The SPSS (statistical package for the social science) software was used to analyze the relationship between the chicken eggs hatching rate and the different injection sites or the different dosages. The experimental results showed that there were significant differences on egg hatching rates among the different injection sites and doses (P
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المؤلفون: Tao Huang, Chengjuan Zhang, Shengze Zhang, Yingjie Wang, Xianfu Sun, Zhenzhen Liu, Qiang Zhang
المصدر: Cell Cycle
مصطلحات موضوعية: 0301 basic medicine, Tube formation, Angiogenesis, Competing endogenous RNA, Cell growth, RNA, Cell Biology, Biology, Reverse transcriptase, 03 medical and health sciences, 030104 developmental biology, 0302 clinical medicine, Real-time polymerase chain reaction, Downregulation and upregulation, 030220 oncology & carcinogenesis, Cancer research, Molecular Biology, Developmental Biology, Research Paper
الوصف: Background: Breast cancer (BC) is a common invasive malignancy in women with unclear etiology. A recent study suggested that long non-coding RNA (lncRNA), LINC00968 had a tumor-promoting effect in cancer. However, the role of LINC00968 in BC remains unclear. Therefore, we conducted the present study to determine the effect of LINC00968 in BC and its underlying mechanism. Methods: The expression of LINC00968 and hsa-miR-423-5p in BC tissues and cells was determined using reverse transcription quantitative polymerase chain reaction and western blot analysis. Dual luciferase reporter, RNA pull-down and RNA immunoprecipitation assays were used to determine the relationship among LINC00968, PROX1 and hsa-miR-423-5p. Gain- and loss-function approaches were utilized to examine the effects of LINC00968, PROX1 and hsa-miR-423-5p on cell proliferation, migration, tube formation in vitro; and tumor growth and angiogenesis in vivo. Results: LINC00968 expression reduced while hsa-miR-423-5p increased in BC tissues relative to adjacent normal tissues. Overexpression of LINC00968 was observed to inhibit BC cell proliferation, migration and tube formation abilities in vitro as well as tumor growth in vivo through inhibition of hsa-miR-423-5p. And hsa-miR-423-5p mediated BC cellular functions and tumor growth through down-regulating PROX1. LINC00968 was identified as a competing endogenous RNA to upregulate PROX1 by downregulating hsa-miR-423-5p. More importantly, it was found that LINC00968 increased PROX1 expression in vivo in a concentration-dependent manner. Conclusion: Taken together, this study suggests that LINC00968 inhibits the progression of BC through impeding hsa-miR-423-5p-mediated PROX1 inhibition. LINC00968 may be a potential therapeutic target for BC therapy that warrants further studies.
URL الوصول: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::113263f42e535bcf8cc0b863dcae02f4
https://europepmc.org/articles/PMC6681781/ -
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المؤلفون: Li Chen, Shichang Zhang, Yingjie Wang, Lu Yang, Jiexin Zhang, Guoying Zhang
المصدر: Stem Cells International
Stem Cells International, Vol 2018 (2018)مصطلحات موضوعية: 0301 basic medicine, Liver injury, lcsh:Internal medicine, Article Subject, Chemistry, Cell, Mesenchymal stem cell, Cell Biology, medicine.disease, In vitro, Andrology, 03 medical and health sciences, chemistry.chemical_compound, 030104 developmental biology, medicine.anatomical_structure, Apoptosis, In vivo, Lactate dehydrogenase, medicine, Viability assay, lcsh:RC31-1245, Molecular Biology, Research Article
الوصف: Mesenchymal stem cells (MSCs) and hepatocytes are two attractive sources of cell-based therapies for acute liver failure (ALF). The cotransplantation of hepatocytes with MSCs can improve the therapeutic performance for the treatment of ALF. However, the therapeutic potential of conditioned medium (CM) derived from MSCs cocultured with hepatocytes (MSC-H-CM) remains unclear. The purpose of this study was to investigate the effects of MSC-H-CM on damaged hepatocytes in vitro and on D-galactosamine-induced ALF in vivo. D-Galactosamine-treated L02 cells cultured in MSC-H-CM exhibited higher of cell viability and total protein synthesis than L02 cells cultured in MSC-CM, CM derived from hepatocytes (H-CM), MSC-CM + H-CM, or with nonconditioned medium (NCM). Lactate dehydrogenase and aspartate aminotransferase levels were lower in the supernatant of damaged L02 cells cultured in MSC-H-CM than in that of L02 cells cultured in other types of CM. The lowest percentage of apoptotic cells was observed after the MSC-H-CM treatment. When CM was injected into the tail vein of rats with ALF, MSC-H-CM was the most successful at preventing the release of liver injury biomarkers and in promoting the recovery of liver structure. The greatest survival rate 7 days after the first treatment was observed in the MSC-H-CM-treated rats. Our results reveal that the delivery of MSC-H-CM could be a novel strategy for integrating the therapeutic potentials of hepatocytes and MSCs for the treatment of ALF.
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