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Parp 1 mice

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PARP-1−/− mice are genetically modified mice that have a disruption or knockout of the PARP-1 gene. PARP-1 is an enzyme involved in various cellular processes, including DNA repair. The absence of PARP-1 in these mice can be used to study the impact of PARP-1 deficiency on biological functions.

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Lab products found in correlation

Accu chek active blood glucose monitor, by Roche (1 mentions) Streptozotocin (stz), by Merck Group (1 mentions) Abt 888, by Selleck Chemicals (1 mentions)

5 protocols using parp 1 mice

1

Generation of PARP-1 Knockout Mouse Models

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PARP-1−/− mice were obtained from the Jackson Laboratory. PARP-1f/f mice and Stat1f/f mice were generated by View Solid Biotechnology Inc. under the combined use of CRISPR/Cas9 and Cre/LoxP. SMACre and lyzMCre transgenic mice were kindly provided by Dr. Wen-cheng Zhang. ApoE−/−PARP-1−/− were generated by crossing PARP-1−/− mice with ApoE−/− mice. VSMC- or macrophage-specific PARP-1 deletion mice on an ApoE−/− background were generated by crossing floxed mice with SMACre or lyzMCre mice, and then crossbreeding with ApoE−/− mice to generate ApoE−/−/PARP-1f/f/SMACre, ApoE−/−/PARP-1f/f/lyzMCre.
Li P., Wang Y., Liu X., Liu B., Wang Z.Y., Xie F., Qiao W., Liang E.S., Lu Q.H, & Zhang M.X. (2020). Loss of PARP-1 attenuates diabetic arteriosclerotic calcification via Stat1/Runx2 axis. Cell Death & Disease, 11(1), 22.
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2

Inducing Diabetes in C57BL/6 and PARP-1-/- Mice

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To induce diabetes, male C57BL/6 (WT) mice or PARP-1−/− mice (10 weeks old, Jackson Laboratories, ME, USA) were treated with STZ (sigma, 50mg/kg in citrate buffer, pH 4.5) by intraperitoneal injection for 5 consecutive days [26 (link)], while the control animals (male C57BL/6 mice) received the same volume of citrate buffer. Mouse tail vein blood glucose levels were monitored by analysis with the Roche Accu-Chek Active blood glucose monitor. The mice with a fasting blood glucose concentration >11.1 mmol/l were considered diabetic. Mice were housed in a pathogen-free animal care facility and allowed free access to food and water. PARP-1−/− mice were genotyped by PCR (Supplementary Figure 1).
Qin W.D., Liu G.L., Wang J., Wang H., Zhang J.N., Zhang F., Ma Y., Ji X.Y., Li C, & Zhang M.X. (2016). Poly(ADP-ribose) polymerase 1 inhibition protects cardiomyocytes from inflammation and apoptosis in diabetic cardiomyopathy. Oncotarget, 7(24), 35618-35631.
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3

PARP-1 Knockout Mice Protocol

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Studies were approved by the San Francisco Veterans Affairs Medical Center animal studies committee and follow the NIH guidelines for humane care of animals. PARP-1−/− mice were initially obtained from the Jackson Laboratory (Bar Harbor, ME) and subsequently bred for more than 10 generations onto the C57BL/6 background. Wild-type C57BL/6 mice were obtained from Simonsen Labs (Gilroy, CA). Studies using adult mice employed males, age 3–4 months. Animals were housed on a 12h light/dark cycle with free access to food and water.
Xu J., Wang H., Won S.J., Basu J., Kapfhamer D, & Swanson R.A. (2016). Microglial activation induced by the alarmin S100B is regulated by poly(ADP-ribose) polymerase-1. Glia, 64(11), 1869-1878.
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4

Sensitizing Mice to Methylmethane Sulfonate

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Parp1−/− mice were purchased from Jackson Laboratories [64 (link)]. Aag transgenic (AagTg) mice were described previously [12 (link), 13 (link), 65 (link)]. All experiments were performed in mixed background mice (C57Bl/6J:129S) unless otherwise stated. All animal procedures were performed according the NIH guide for the Care and Use of Laboratory Animals.
Approximate LD50 was determined as in Deichmann and LeBlanc [66 ]. MMS was injected intraperitoneally. ABT-888 (10 mg/kg, Selleck Chemicals Inc) was administered by oral gavage 1 hour before and 5 days after MMS treatment. For estrogen treatment, 17b-estradiol pellets (E2, 0.1 mg/21 days release, Innovative Research of America) were implanted s.c. in the dorsal neck region of adult male mice. MMS was administered 3 days after implants.
Calvo J.A., Allocca M., Fake K.R., Muthupalani S., Corrigan J.J., Bronson R.T, & Samson L.D. (2016). Parp1 protects against Aag-dependent alkylation-induced nephrotoxicity in a sex-dependent manner. Oncotarget, 7(29), 44950-44965.
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5

Genetically Modified Mouse Models

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The Abcc6−/− mouse was generated and described previously (Klement et al., 2005 (link)). The Parp1−/− mice, described previously (Waymire et al., 1995 (link)), were obtained from The Jackson Laboratory (Bar Harbor, ME). The Abcc6 and Parp1 double mutant mice were generated by intercrossing Abcc6−/− mice with Parp1−/− mice. In the proof-of-concept genetic study, the wild-type, Abcc6−/−Parp1+/+, and Abcc6−/−Parp1−/− mice were fed a standard rodent diet (Lab Diet 5010; PMI Nutrition, Brentwood, MO) throughout the experiments. In the minocycline treatment experiments, Abcc6−/− mice were treated with 0.5 mg/mL minocycline administered in the drinking water. This dose corresponds to 100 mg/kg body weight/day, assuming that a 20-g mouse consumes 4 mL of water per day. The treatment was initiated in mice at 4 weeks of age and continued for an additional 8 weeks. All mice were killed at 12 weeks of age for analysis. The protocols were approved by the Institutional Animal Care and Use Committee of Thomas Jefferson University.
Huang J., Ralph D., Boraldi F., Quaglino D., Uitto J, & Li Q. (2022). Inhibition of the DNA Damage Response Attenuates Ectopic Calcification in Pseudoxanthoma Elasticum. The Journal of investigative dermatology, 142(8), 2140-2148.e1.
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