InVivoPure pH 8.0 Dilution Buffer

Catalog #IP0080
Product Citations:
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Product Details

InVivoPure™ dilution buffers are specifically formulated and tested to satisfy the stringent requirements for in vivo applications. They are extremely low in endotoxin, have been screened for murine pathogens, tested in animal models for toxicity and are formulated with respect to buffer composition and pH to satisfy the requirements of Bio X Cell’s antibodies.

Specifications

Endotoxin <0.5 EU/mL (<0.0005EU/μL)
Endotoxin level is determined using an LAL gel clotting test
Sterility 0.2 μM filtered
Murine Pathogen Tests Mouse Norovirus: Negative
Mouse Parvovirus: Negative
Mouse Minute Virus: Negative
Mouse Hepatitis Virus: Negative
Reovirus Screen: Negative
Lymphocytic Choriomeningitis virus: Negative
Lactate Dehydrogenase-Elevating Virus: Negative
Mouse Rotavirus: Negative
Theiler’s Murine Encephalomyelitis: Negative
Ectromelia/Mousepox Virus: Negative
Hantavirus: Negative
Polyoma Virus: Negative
Mouse Adenovirus: Negative
Sendai Virus: Negative
Mycoplasma Pulmonis: Negative
Pneumonia Virus of Mice: Negative
Mouse Cytomegalovirus: Negative
K Virus: Negative
Toxicity Test Results Nontoxic and nonantigenic in animal models
Concentration 1X
Volume 50 ml
Composition 35 mM Na2HPO4 1.7 mM NaH2PO4 136 mM NaCl
This buffer does not contain calcium, magnesium, phenol red, or preservatives such as azide.
Keep contents sterile. Open only in a biological safety cabinet.
Storage 4°C
    • Genetics
    • ,
    IFN-γ blockade after genetic inhibition of PD-1 aggravates skeletal muscle damage and impairs skeletal muscle regeneration.

    In Cellular Molecular Biology Letters on 4 April 2023 by Zhuang, S., Russell, A., et al.

    PubMed

    Innate immune responses play essential roles in skeletal muscle recovery after injury. Programmed cell death protein 1 (PD-1) contributes to skeletal muscle regeneration by promoting macrophage proinflammatory to anti-inflammatory phenotype transition. Interferon (IFN)-γ induces proinflammatory macrophages that appear to hinder myogenesis in vitro. Therefore, we tested the hypothesis that blocking IFN-γ in PD-1 knockout mice may dampen inflammation and promote skeletal muscle regeneration via regulating the macrophage phenotype and neutrophils. Anti-IFN-γ antibody was administered in PD-1 knockout mice, and cardiotoxin (CTX) injection was performed to induce acute skeletal muscle injury. Hematoxylin and eosin (HE) staining was used to view morphological changes of injured and regenerated skeletal muscle. Masson's trichrome staining was used to assess the degree of fibrosis. Gene expressions of proinflammatory and anti-inflammatory factors, fibrosis-related factors, and myogenic regulator factors were determined by real-time polymerase chain reaction (PCR). Changes in macrophage phenotype were examined by western blot and real-time PCR. Immunofluorescence was used to detect the accumulation of proinflammatory macrophages, anti-inflammatory macrophages, and neutrophils. IFN-γ blockade in PD-1 knockout mice did not alleviate skeletal muscle damage or improve regeneration following acute cardiotoxin-induced injury. Instead, it exacerbated skeletal muscle inflammation and fibrosis, and impaired regeneration via inhibiting macrophage accumulation, blocking macrophage proinflammatory to anti-inflammatory transition, and enhancing infiltration of neutrophils. IFN-γ is crucial for efficient skeletal muscle regeneration in the absence of PD-1. © 2023. The Author(s).