scholarly journals Atorvastatin Ester Regulates Lipid Metabolism in Hyperlipidemia Rats via the PPAR-Signaling Pathway and HMGCR Expression in the Liver

2021 ◽  
Vol 22 (20) ◽  
pp. 11107
Author(s):  
Nan Hu ◽  
Chunyun Chen ◽  
Jinhui Wang ◽  
Jian Huang ◽  
Dahong Yao ◽  
...  
Keyword(s):  
Lipid Metabolism ◽  
Signaling Pathway ◽  
Rna Sequencing ◽  
Western Blotting ◽  
Rat Liver ◽  
Lipid Level ◽  
Lipid Lowering ◽  
Intragastric Administration ◽  
Qrt Pcr ◽  
Ppar Signaling

Atorvastatin ester (Ate) is a structural trim of atorvastatin that can regulate hyperlipidemia. The purpose of this study was to evaluate the lipid-lowering effect of Ate. Male Sprague Dawley (SD) rats were fed a high-fat diet for seven months and used as a hyperlipidemia model. The lipid level and liver function of the hyperlipidemia rats were studied by the levels of TG, TC, LDL, HDL, ALT, and AST in serum after intragastric administration with different doses of Ate. HE staining was used to observe the pathological changes of the rat liver and gastrocnemius muscle. The lipid deposits in the liver of rats were observed by staining with ORO. The genes in the rat liver were sequenced by RNA-sequencing. The results of the RNA-sequencing were further examined by qRT-PCR and western blotting. Biochemical test results indicated that Ate could obviously improve the metabolic disorder and reduce both the ALT and AST levels in serum of the hyperlipidemia rats. Pathological results showed that Ate could improve HFD-induced lipid deposition and had no muscle toxicity. The RNA-sequencing results suggested that Ate affected liver lipid metabolism and cholesterol, metabolism in the hyperlipidemia-model rats may vary via the PPAR-signaling pathway. The western blotting and qRT-PCR results demonstrated the Ate-regulated lipid metabolism in the hyperlipidemia model through the PPAR-signaling pathway and HMGCR expression. In brief, Ate can significantly regulate the blood lipid level of the model rats, which may be achieved by regulating the PPAR-signaling pathway and HMGCR gene expression. 

scholarly journals Acetyl-CoA Synthetase 2 Promotes Cell Migration and Invasion of Renal Cell Carcinoma by Upregulating Lysosomal-Associated Membrane Protein 1 Expression

2018 ◽  
Vol 45 (3) ◽  
pp. 984-992 ◽  
Author(s):  
Lv Yao ◽  
Xiaoqiang Guo ◽  
Yaoting Gui
Keyword(s):  
Cell Proliferation ◽  
Cell Migration ◽  
Lipid Metabolism ◽  
Western Blotting ◽  
Renal Cell ◽  
Migration And Invasion ◽  
Cancer Tissue ◽  
Acetyl Coa ◽  
Cell Migration And Invasion ◽  
Qrt Pcr

Background/Aims: Reprogramming energy metabolism is an emerging hallmark of many cancers, and this alteration is especially evident in renal cell carcinomas (RCCs). However, few studies have been conducted on lipid metabolism. This study investigated the function and mechanism of lipid metabolism-related acetyl-CoA synthetase 2 (ACSS2) in RCC development, cell migration and invasion. Methods: Quantitative real-time PCR (qRT-PCR) was used to determine the expression of ACSS2 in cancer tissue and adjacent tissue. The inhibition of ACSS2 expression was achieved by RNA interference, which was confirmed by qRT-PCR and Western blotting. Cell proliferation and apoptosis were detected by a CCK8 assay and a flow cytometry analysis, respectively. Cell migration and invasion were determined by the scratch and transwell assays. Following the knockdown of ACSS2 expression, the expression of the autophagy-related factor LAMP1 was measured by qRT-PCR and Western blotting. Results: Compared to adjacent tissues, ACSS2 expression was upregulated in RCC cancer tissues and positively correlated with metastasis. Inhibition of ACSS2 had no effect on RCC cell proliferation or apoptosis. However, decreased ACSS2 expression was found to inhibit RCC cell migration and invasion. ACSS2 was determined to promote the expression of LAMP1, which can also promote cell migration. This pathway may be considered a potential mechanism through which ACSS2 participates in RCC development. Conclusion: These data suggest that ACSS2 is an important factor for promoting RCC development and is essential for cell migration and invasion, which it promotes by increasing the expression of LAMP1. Taken together, these findings reveal a potential target for the diagnosis and treatment of RCC.

scholarly journals Based on Network Pharmacology and RNA Sequencing Techniques to Explore the Molecular Mechanism of Huatan Jiangzhuo Decoction for Treating Hyperlipidemia

2021 ◽  
Vol 2021 ◽  
pp. 1-16
Author(s):  
Xiaowen Zhou ◽  
Zhenqian Yan ◽  
Yaxin Wang ◽  
Qi Ren ◽  
Xiaoqi Liu ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Lipid Metabolism ◽  
Rna Sequencing ◽  
Therapeutic Effect ◽  
Animal Experiment ◽  
Kegg Pathway ◽  
Network Pharmacology ◽  
Network Construction ◽  
Pathway Enrichment ◽  
Qrt Pcr

Background. Hyperlipidemia, due to the practice of unhealthy lifestyles of modern people, has been a disturbance to a large portion of population worldwide. Recently, several scholars have turned their attention to Chinese medicine (CM) to seek out a lipid-lowering approach with high efficiency and low toxicity. This study aimed to explore the mechanism of Huatan Jiangzhuo decoction (HTJZD, a prescription of CM) in the treatment of hyperlipidemia and to determine the major regulation pathways and potential key targets involved in the treatment process. Methods. Data on the compounds of HTJZD, compound-related targets (C-T), and known disease-related targets (D-T) were collected from databases. The intersection targets (I-T) between C-T and D-T were filtered again to acquire the selected targets (S-T) according to the specific index. Gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment, as well as network construction, were applied to predict the putative mechanisms of HTJZD in treating hyperlipidemia. Thereafter, an animal experiment was conducted to validate the therapeutic effect of HTJZD. In addition, regulated differentially expressed genes (DEGs) were processed from the RNA sequencing analysis results. Common genes found between regulated DEGs and S-T were analyzed by KEGG pathway enrichment to select the key targets. Lastly, key targets were validated by real-time quantitative reverse transcription PCR (qRT-PCR) analysis. Results. A total of 210 S-T were filtered out for enrichment analysis and network construction. The enrichment results showed that HTJZD may exert an effect on hyperlipidemia through the regulation of lipid metabolism and insulin resistance. The networks predict that the therapeutic effect of HTJZD may be based on the composite pharmacological action of these active compounds. The animal experiment results verify that HTJZD can inhibit dyslipidemia in rats with hyperlipidemia, suppress lipid accumulation in the liver, and reverse the expression of 202 DEGs, which presented an opposite trend in the model and HTJZD groups. Six targets were selected from the common targets between 210 S-T and 202 regulated DEGs, and the qRT-PCR results showed that HTJZD could effectively reverse Srebp-1c, Cyp3a9, and Insr mRNA expression (P < 0.01). Conclusion. In brief, network pharmacology predicted that HTJZD exerts a therapeutic effect on hyperlipidemia. The animal experimental results confirmed that HTJZD suppressed the pathological process induced by hyperlipidemia by regulating the expression of targets involved in lipid metabolism and insulin resistance.

scholarly journals Identification of molecular regulation on difference of lipid deposition in dedifferentiated preadipocytes from different chicken tissues

2021 ◽  
Author(s):  
zheng ma ◽  
Na Luo ◽  
Lu Liu ◽  
Huanxian Cui ◽  
Jing Li ◽  
...  
Keyword(s):  
Fatty Acid ◽  
Lipid Metabolism ◽  
Signaling Pathway ◽  
Lipid Content ◽  
Regulatory Network ◽  
Fatty Acid Transport ◽  
Lipid Deposition ◽  
Ppar Signaling ◽  
The Difference

Abstract Background: The body distribution with high intramuscular fat and low abdominal fat is ideal goal for broiler breeding. Preadipocytes with different origins have differences in metabolism and gene expression. This transcriptome analysis of intramuscular preadipocytes (DIMPs) and adipose tissue-derived preadipocytes (DAFPs) is aim to explore the characteristics in lipid deposition of different chicken preadipocytes by dedifferentiation in vitro. Results: Compared to DAFPs, the total lipid content was decreased (P <0.05) in DIMFPs after two days with 100% confluence. Moreover, 72 DEGs related to lipid metabolism were screened, which are involved in the adipocyte differentiation, fatty acid transport and fatty acid synthesis, lipid stabilization, and lipolysis. Among the 72 DEGs, 19 DEGs were enriched in the PPAR signaling pathway, indicating a main contribution to the regulation of the difference of lipid deposition between DAFPs and DIMFPs. Among these 19 genes, the representative APOA1, ADIPOQ, FABP3, FABP4, FABP7, HMGCS2, LPL and RXRG genes were down-regulated, but ACSL1, FABP5, PCK2, PDPK1, PPARG, SCD, SCD5, SLC27A6 genes were up-regulated (P < 0.05 or P < 0.01) in the DIMFPs. In addition, the well-known pathways affecting lipid metabolism (MAPK-, TGF beta-, Calcium-, PPAR signaling pathway) and the pathways related to cell communication were enriched, which may also contribute to the regulation of lipid deposition. Finally, the regulatory network for the difference of lipid deposition between chicken DAFPs and DIMFPs were proposed based on the above information.Conclusions: Our data suggested the difference of lipid deposition between DIMPs and DAFPs of chicken in vitro, and proposed the molecular regulatory network for the difference of lipid deposition between chicken DAFPs and DIMFPs. The lipid content was significantly increased in DAFPs by the direct mediation of PPAR signaling pathways. These findings provide new insights into the regulation of tissue-specific fat deposition and optimizing body fat distribution in broilers.

scholarly journals Transcriptome Analysis of EnJSRV-Env on the Inhibition of Cell Proliferation

2021 ◽  
Author(s):  
Xiaojuan Wang ◽  
Liang Zhang ◽  
Shuying Liu
Keyword(s):  
Signaling Pathway ◽  
Western Blotting ◽  
Hela Cells ◽  
Transcriptome Analysis ◽  
Endogenous Retroviruses ◽  
Rna Seq ◽  
Quantitative Real Time Pcr ◽  
Placental Development ◽  
Qrt Pcr ◽  
Proliferation Ability

Abstract Background Endogenous retroviruses (ERVs) exert important biological roles, such as mammalian placental development and suppression of the infection of exogenous retrovirus. In addition, ERVs could also inhibit the proliferation of cell. The envelope-protein (Env) of endogenous Jaagsiekte sheep retroviruses (enJSRVs) possesses fusogenic activity, which promoted the formation of nonproliferative multinucleated syncytiotrophoblasts. Methods The proliferation of HeLa cells was detected by MTT. Six samples were extracted for RNA-seq transcriptome analysis. Quantitative real-time PCR (qRT-PCR) and western blotting were employed for the validation of interested target. Results enJSRV-Env transfection inhibited the proliferation ability of Hela cells and 170 differentially expressed genes (DEGs) were obtained by RNA-seq analysis. Among these, 5 DEGs (BHLHE41, CCN1, DLX2, DUSP6 and SH2D5) were validated by qRT-PCR, which closely related with proliferation. Western blotting analysis showed that the expression of DUSP6 and p-ERK1/2 was decreased, which suggested that ERK1/2 signaling pathway may be involved in enJSRV-Env transfection. Conclusions enJSRV-Env transfection inhibited the proliferation of Hela cells, probably via DUSP6 and ERK1/2 signaling pathway.

scholarly journals Screening for differentially expressed circRNAs in ischemic stroke by RNA sequencing

BMC Neurology ◽  
2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Duncan Wei ◽  
Jian Chen ◽  
Xiaopu Chen ◽  
Shaoyan Wu ◽  
Zhaolin Chen ◽  
...  
Keyword(s):  
Ischemic Stroke ◽  
Signaling Pathway ◽  
Rna Sequencing ◽  
Cell Receptor ◽  
Differentially Expressed ◽  
Receptor Signaling ◽  
Qrt Pcr ◽  
Receptor Signaling Pathway ◽  
Cell Receptor Signaling ◽  
Host Genes

Abstract Background Ischemic stroke is a disease with high rate of death and disability worldwide. CircRNAs, as a novel type of non-coding RNAs, lacking 5’ caps and 3’ poly-A tails, has been associated with ischemic stroke. This study aimed to investigate key circRNAs related to ischemic stroke. Methods RNA sequencing was performed obtain the circRNA expression profiles from peripheral whole blood of three ischemic stroke patients and three healthy individuals. Through bioinformatic analysis, differentially expressed circRNAs (DEcircRNAs) were identified, and GO and pathway analyses for the host genes of DEcircRNAs were conducted. The expression levels of selected circRNAs were analyzed with qRT-PCR. To further explore the functions of key circRNAs, a DEcircRNA-miRNA interaction network was constructed. Results A total of 736 DEcircRNAs were detected in ischemic stroke. Functional annotation of host genes of DEcircRNAs revealed several significantly enriched pathways, including Fc epsilon RI signaling pathway, B cell receptor signaling pathway, and T cell receptor signaling pathway. The qRT-PCR results were largely in keeping with our RNA-seq data. The ROC curve analyses indicated that hsa_circ_0000745, hsa_circ_0001459, hsa_circ_0003694 and hsa_circ_0007706 with relatively high diagnostic value. A circRNA-miRNA network, including 1544 circRNA-miRNA pairs, 456 circRNAs and 4 miRNAs, was obtained. Conclusions The results of our study may help to elucidate the specific mechanism underlying ischemic stroke.

scholarly journals Effects of Thalidomide on the Expression of Adhesion Molecules in Rat Liver Cirrhosis

2006 ◽  
Vol 2006 ◽  
pp. 1-10 ◽  
Author(s):  
Peng Lv ◽  
Shelley Chireyath Paul ◽  
Yanjv Xiao ◽  
Shiquan Liu ◽  
Hesheng Luo
Keyword(s):  
Liver Cirrhosis ◽  
Liver Fibrosis ◽  
Signaling Pathway ◽  
Adhesion Molecules ◽  
Rat Liver ◽  
Intraperitoneal Injection ◽  
Wistar Rats ◽  
High Dose ◽  
Intragastric Administration ◽  
Liver Histopathology

This study was to evaluate the effects of thalidomide on expression of adhesion molecules in liver cirrhosis. The cirrhosis was induced in Wistar rats by intraperitoneal injection ofCCl4, and thalidomide (10 mg/kg/day or 100 mg/kg/day) was given by intragastric administration for 8 weeks. Liver histopathology and immunohistochemistry were significantly improved and the expressions of ICAM-1, VCAM-1, E-selectin, and TNF-αmRNA and protein were decreased significantly in rats treated with a high dose of thalidomide. Close positive correlation was observed in the expression of the TNF-αmRNA and that of ICAM-1, VCAM-1, and E-selectin mRNA, respectively. These results indicate that thalidomide exerts its effect on the downregulation of adhesion molecules via TNF-αsignaling pathway to inhibit liver fibrosis.

scholarly journals Lipopolysaccharide-Induced Transcriptional Changes in LBP-Deficient Rat and Its Possible Implications for Liver Dysregulation during Sepsis

2021 ◽  
Vol 2021 ◽  
pp. 1-14
Author(s):  
Zhixiang He ◽  
Zichen Song ◽  
Leilei Meng ◽  
Wenhui Cheng ◽  
Fan Huang ◽  
...  
Keyword(s):  
Inflammatory Response ◽  
Signaling Pathway ◽  
Rna Sequencing ◽  
Liver Tissue ◽  
Serum Lactate ◽  
Functional Enrichment ◽  
Serum Lactate Dehydrogenase ◽  
Peroxisome Proliferator ◽  
Multiple Time ◽  
Ppar Signaling

Sepsis is an organ dysfunction caused by the dysregulated inflammatory response to infection. Lipopolysaccharide-binding protein (LBP) binds to lipopolysaccharide (LPS) and modulates the inflammatory response. A rare systematic study has been reported to detect the effect of LBP gene during LPS-induced sepsis. Herein, we explored the RNA sequencing technology to profile the transcriptomic changes in liver tissue between LBP-deficient rats and WT rats at multiple time points after LPS administration. We proceeded RNA sequencing of liver tissue to search differentially expressed genes (DEGs) and enriched biological processes and pathways between WT and LBP-deficient groups at 0 h, 6 h, and 24 h. In total, 168, 284, and 307 DEGs were identified at 0 h, 6 h, and 24 h, respectively, including Lrp5, Cyp7a1, Nfkbiz, Sigmar1, Fabp7, and Hao1, which are related to the inflammatory or lipid-related process. Functional enrichment analysis revealed that inflammatory response to LPS mediated by Ifng, Cxcl10, Serpine1, and Lbp was enhanced at 6 h, while lipid-related metabolism associated with C5, Cyp4a1, and Eci1 was enriched at 24 h after LPS administration in the WT samples. The inflammatory process was not found when the LBP gene was knocked out; lipid-related metabolic process and peroxisome proliferator-activated receptor (PPAR) signaling pathway mediated by Dhrs7b and Tysnd1 were significantly activated in LBP-deficient samples. Our study suggested that the invading LPS may interplay with LBP to activate the nuclear factor kappa B (NF-κB) signaling pathway and trigger uncontrolled inflammatory response. However, when inhibiting the activity of NF-κB, lipid-related metabolism would make bacteria removal via the effect on the PPAR signaling pathway in the absence of LBP gene. We also compared the serum lactate dehydrogenase (LDH) and alkaline phosphatase (ALP) levels using the biochemistry analyzer and analyzed the expression of high mobility group box 1 (HMGB1) and cleaved-caspase 3 with immunohistochemistry, which further validated our conclusion.

scholarly journals RNA-sequencing reveals the expression profiles of tsRNAs and their potential carcinogenic role in cholangiocarcinoma

2021 ◽  
Author(s):  
Li-rong Yan ◽  
Ang Wang ◽  
Qian Xu ◽  
Ben-gang Wang
Keyword(s):  
Signaling Pathway ◽  
Rna Sequencing ◽  
High Throughput ◽  
Target Genes ◽  
Expression Profiles ◽  
Biological Effects ◽  
Differentially Expressed ◽  
Rna Seq ◽  
Normal Tissues ◽  
Qrt Pcr

Abstract Background Recently, the incidence of cholangiocarcinoma (CCA) has gradually increased. As CCA has a poor prognosis, the ideal survival rate is scarce for patients. The abnormal expressed tsRNAs may regulate the progression of a variety of tumors, and tsRNAs is expected to become a new diagnostic biomarker of cancer. However, the expression of tsRNAs is obscure and should be elucidated in CCA. Methods High-throughput RNA sequencing technology (RNA-seq) was utilized to determine the overall expression profiles of tsRNAs in 3 pairs CCA and adjacent normal tissues and to screen the tsRNAs that were differentially expressed. The target genes of dysregulated tsRNAs were predicted and the biological effects and potential signaling pathways of these target genes were explored by Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analyses. Quantitative real-time polymerase chain reaction (qRT-PCR) was used to validate 11 differentially expressed tRFs with 12 pairs CCA and adjacent normal tissues. Results High-throughput RNA-seq totally demonstrated 535 dysregulated tsRNAs, of which 241 tsRNAs were upregulated and 294 tsRNAs were downregulated in CCA compared with adjacent normal tissues (|log2 (fold change) |≥1 and P value < 0.05). GO and KEGG enrichment analyses indicated that the target genes of dysregulated tRFs (tRF-34-JJ6RRNLIK898HR, tRF-38-0668K87SERM492V and tRF-39-0668K87SERM492E2) were mainly enriched in the Notch signaling pathway, Hippo signaling pathway, cAMP signaling pathway and in growth hormone synthesis, secretion and action, etc. qRT-PCR result showed that tRF-34-JJ6RRNLIK898HR/tRF-38-0668K87SERM492V/tRF-39-0668K87SERM492E2 was down-regulated (P = 0.021) and tRF-20-LE2WMK81 was up-regulated in CCA (P = 0.033). Conclusion Differentially expressed tRFs in CCA are enriched in many pathways associated with neoplasms, which may impact the tumor progression and have potential to be diagnostic biomarkers and therapeutic targets of CCA.

scholarly journals RIG-I, a novel DAMPs sensor for myoglobin activates NF-κB/caspase-3 signaling in CS-AKI model

2021 ◽  
Vol 8 (1) ◽  
Author(s):  
Peng-Tao Wang ◽  
Ning Li ◽  
Xin-Yue Wang ◽  
Jia-Le Chen ◽  
Chen-Hao Geng ◽  
...  
Keyword(s):  
Signaling Pathway ◽  
Rna Sequencing ◽  
Western Blotting ◽  
Caspase 3 ◽  
Rat Kidney ◽  
Kidney Tissue ◽  
Kidney Injury ◽  
Cellular Level ◽  
Small Interfering Rnas ◽  
Sprague Dawley

Abstract Background Acute kidney injury (AKI) is the main life-threatening complication of crush syndrome (CS), and myoglobin is accepted as the main pathogenic factor. The pattern recognition receptor retinoicacid-inducible gene I (RIG-I) has been reported to exert anti-viral effects function in the innate immune response. However, it is not clear whether RIG-I plays a role in CS-AKI. The present research was carried out to explore the role of RIG-I in CS-AKI. Methods Sprague-Dawley rats were randomly divided into two groups: the sham and CS groups (n = 12). After administration of anesthesia, the double hind limbs of rats in the CS group were put under a pressure of 3 kg for 16 h to mimic crush conditions. The rats in both groups were denied access to food and water. Rats were sacrificed at 12 h or 36 h after pressure was relieved. The successful establishment of the CS-AKI model was confirmed by serum biochemical analysis and renal histological examination. In addition, RNA sequencing was performed on rat kidney tissue to identify molecular pathways involved in CS-AKI. Furthermore, NRK-52E cells were treated with 200 μmol/L ferrous myoglobin to mimic CS-AKI at the cellular level. The cells and cell supernatant samples were collected at 6 h or 24 h. Small interfering RNAs (siRNA) was used to knock down RIG-I expression. The relative expression levels of molecules involved in the RIG-I pathway in rat kidney or cells samples were measured by quantitative Real-time PCR (qPCR), Western blotting analysis, and immunohistochemistry (IHC) staining. Tumor necrosis factor-α (TNF-α) was detected by ELISA. Co-Immunoprecipitation (Co-IP) assays were used to detect the interaction between RIG-I and myoglobin. Results RNA sequencing of CS-AKI rat kidney tissue revealed that the different expression of RIG-I signaling pathway. qPCR, Western blotting, and IHC assays showed that RIG-I, nuclear factor kappa-B (NF-κB) P65, p-P65, and the apoptotic marker caspase-3 and cleaved caspase-3 were up-regulated in the CS group (P < 0.05). However, the levels of interferon regulatory factor 3 (IRF3), p-IRF3 and the antiviral factor interferon-beta (IFN-β) showed no significant changes between the sham and CS groups. Co-IP assays showed the interaction between RIG-I and myoglobin in the kidneys of the CS group. Depletion of RIG-I could alleviate the myoglobin induced expression of apoptosis-associated molecules via the NF-κB/caspase-3 axis. Conclusion RIG-I is a novel damage-associated molecular patterns (DAMPs) sensor for myoglobin and participates in the NF-κB/caspase-3 signaling pathway in CS-AKI. In the development of CS-AKI, specific intervention in the RIG-I pathway might be a potential therapeutic strategy for CS-AKI.

scholarly journals Different expression of lipid metabolism-related genes in Shandong black cattle and Luxi cattle based on transcriptome analysis

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Ruili Liu ◽  
Xianxun Liu ◽  
Xuejin Bai ◽  
Chaozhu Xiao ◽  
Yajuan Dong
Keyword(s):  
Fatty Acids ◽  
Lipid Metabolism ◽  
Wnt Signaling ◽  
Signaling Pathway ◽  
Unsaturated Fatty Acids ◽  
Wnt Signaling Pathway ◽  
Fat Deposition ◽  
Longissimus Dorsi ◽  
Marker Genes ◽  
Ppar Signaling

AbstractTo provide new ideas for improving meat quality and generating new breeds of cattle, the important candidate genes affecting fat deposition in two kinds of cattle were identified. Eighteen months Shandong black cattle (n = 3) and Luxi cattle (n = 3) were randomly assigned into two environmental. The longissimus dorsi muscles of Shandong Black Cattle and Luxi Cattle were collected and analyzed by fatty acid determination, high-throughput sequencing transcriptomics, qRT-PCR expression profile and western blot. The ratio of unsaturated fatty acids to saturated fatty acids was 1.37:1 and 1.24:1 in the muscle tissues of Shandong black cattle and Luxi cattle, respectively. The results of RNA-Seq analysis revealed 1320 DEGs between the longissimus dorsi of Shandong black cattle and Luxi cattle. A total of 867 genes were upregulated, and the other 453 genes were downregulated. With GO enrichment analysis, it was found that the identified DEGs were significantly enriched in regulation of the Wnt signaling pathway, negative regulation of the Wnt signaling pathway, cAMP metabolic process, fat cell differentiation and among other functions. We found that regulation of lipolysis in adipocytes was the significant enrichment pathway of upregulated genes and downregulated genes, PPAR signaling pathway and AMPK signaling pathway are highly representative pathways of lipid metabolism in Shandong black cattle. Network analysis showed that PPARGC1A, ADCY4, ANKRD6, COL1A1, FABP4, ADIPOQ, PLIN1, PLIN2, and LIPE genes were correlated with key loci genes in multiple metabolic pathways. Meanwhile we found that FABP4 and ADIPOQ had 7 common regulatory factors in different genes, which were PLIN1, PLIN2, PPARGC1A, RXRA, PCK1, LEPR, LEP. These genes were involved in regulation of lipolysis in adipocytes, adipocytokine signaling pathway, PPAR signaling pathway. FABP4 and ADIPOQ were selected as important candidate marker genes for fat deposition based on the results.

Sign in / Sign up

Export Citation Format

Share Document