B-hAPOC3 mice

C57BL/6N-Apoc3tm1(APOC3)Bcgen/Bcgen • 112411

B-hAPOC3 mice

Catalog Number
112411
Strain Name
C57BL/6N-Apoc3tm1(APOC3)Bcgen/Bcgen
Strain Background
C57BL/6N
NCBI gene ID
345 (Human)
Aliases
APOCIII, Apo-C3, ApoC-3

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  • Description
  • Phenotypic analysis
  • Efficacy
  • FAQ section

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      Description
      • B-hAPOC3 mice are APOC3 gene-humanized mice generated on a C57BL/6N background for lipid metabolism and APOC3-targeted drug discovery.
      • APOC3, also known as Apo-C3 or APOCIII, is a key apolipoprotein involved in triglyceride-rich lipoprotein metabolism and plasma triglyceride regulation.
      • B-hAPOC3 mice provide an in vivo model for studying triglyceride metabolism, hypertriglyceridemia-related biology, and human APOC3 inhibition.

      Key Advantages

      • Humanized APOC3 mouse model on a C57BL/6N background
      • Human APOC3 protein expression validated in serum by ELISA
      • Human APOC3 mRNA expression validated in liver by RT-PCR
      • Lipid metabolism characterization showed significantly higher triglyceride levels in B-hAPOC3 mice than in wild-type C57BL/6 mice
      • Supports in vivo evaluation of human APOC3-targeted nucleic acid drugs
      • Useful for triglyceride metabolism, dyslipidemia, and APOC3 pharmacology research

      Validation

      • Protein Validation: Human APOC3 protein was detected in serum from homozygous B-hAPOC3 mice by ELISA using a species-specific APOC3 ELISA kit.
      • mRNA Validation: Human APOC3 mRNA was detected in liver RNA from homozygous B-hAPOC3 mice by RT-PCR, while mouse Apoc3 mRNA was detected in wild-type C57BL/6 mice.
      • Lipid Metabolism Validation: Plasma TG, TC, LDL-C, and HDL-C were measured in B-hAPOC3 mice and wild-type C57BL/6 mice, with TG significantly higher in B-hAPOC3 mice.
      • Efficacy Validation: Human APOC3-targeted nucleic acid drugs reduced liver human APOC3 mRNA expression and significantly decreased plasma TG in B-hAPOC3 mice.

      Application

      • Human APOC3-targeted nucleic acid drug evaluation
      • APOC3 inhibition and triglyceride-lowering pharmacology studies
      • Lipid metabolism and dyslipidemia research
      • Hypertriglyceridemia-related preclinical model studies
      • Human APOC3 mRNA and protein expression validation
      • Preclinical evaluation of therapies targeting triglyceride-rich lipoprotein metabolism
      Human APOC3 Protein Expression Analysis

      Strain-specific human APOC3 expression analysis in homozygous B-hAPOC3 mice by ELISA. Serum was isolated from homozygous B-hAPOC3 mice (H/H) and analyzed by ELISA with a species-specific APOC3 ELISA kit. Human APOC3 was detectable in homozygous B-hAPOC3 mice.

      APOC3 mRNA Expression Analysis

      Strain-specific analysis of APOC3 mRNA expression in wild-type C57BL/6 mice and B-hAPOC3 mice by RT-PCR. Liver RNA was isolated from wild-type C57BL/6 mice (+/+) and homozygous B-hAPOC3 mice (H/H). cDNA libraries were synthesized by reverse transcription and followed by PCR with mouse or human APOC3 primers. Mouse Apoc3 mRNA was detectable in wild-type C57BL/6 mice. Human APOC3 mRNA was detectable in homozygous B-hAPOC3 mice but not in wild-type mice.

      Lipid Metabolism Analysis with Human APOC3 Expression

      Lipid metabolism analysis in B-hAPOC3 mice. Plasma concentrations of TG, TC, LDL-C, and HDL-C in B-hAPOC3 mice and wild-type C57BL/6 mice (5-week-old) were analyzed. TG in B-hAPOC3 mice was significantly higher than that in wild-type C57BL/6 mice. TG: triglycerides; TC: total cholesterol; HDL-C: high-density lipoprotein cholesterol; LDL-C: low-density lipoprotein cholesterol.

      Inhibitory Efficiency of Nucleic Acid Drugs against Human APOC3

      Inhibitory efficiency of nucleic acid drugs against human APOC3 in B-hAPOC3 mice. B-hAPOC3 mice were randomly divided into two groups. Human APOC3-targeted nucleic acid drugs and PBS were administered individually, with drug dosage calculated according to body weight. Mice were sacrificed on day 14, and liver tissue was collected to detect human APOC3 mRNA by qPCR. Compared with control group G1, treatment group G2 showed a significant decrease in TG and reduced human APOC3 mRNA expression. The inhibition rate in the treatment group was 73.4%.

      FAQ section

      Q1: What are B-hAPOC3 mice?

      B-hAPOC3 mice are APOC3 gene-humanized mice on a C57BL/6N background, developed for lipid metabolism research and in vivo evaluation of human APOC3-targeted therapeutics.

      Q2: Why is APOC3 important?

      APOC3 is an apolipoprotein involved in triglyceride-rich lipoprotein metabolism and plasma triglyceride regulation, making APOC3 an important target for dyslipidemia and hypertriglyceridemia research.

      Q3: How was human APOC3 expression validated?

      Human APOC3 protein was validated in serum by ELISA, and human APOC3 mRNA was validated in liver by RT-PCR in homozygous B-hAPOC3 mice.

      Q4: Can B-hAPOC3 mice be used for nucleic acid drug studies?

      Yes. Human APOC3-targeted nucleic acid drugs significantly reduced plasma TG and decreased liver human APOC3 mRNA expression in B-hAPOC3 mice, with a reported inhibition rate of 73.4%.

      Q5: What are the main applications of B-hAPOC3 mice?

      Applications include APOC3-targeted nucleic acid drug evaluation, triglyceride-lowering pharmacology, lipid metabolism studies, dyslipidemia research, and human APOC3 expression analysis.

      * When publishing results obtained using this animal model, please acknowledge the source as follows: The animal model [B-hAPOC3 mice] (Cat# 112411) was purchased from Biocytogen.