Cat.No. : AAV00104Z
Titer: ≥1x10^12 GC/mL / ≥1x10^13 GC/mL Size: 30 ul/100 ul/500 ul/1 ml
Serotype: AAV Serotype 9 Storage: -80 ℃
| Cat. No. | AAV00104Z |
| Description | AAV (Serotype 9) is the serotype 9 AAV with CMV promoter with no insert gene. Used as a control. |
| Serotype | AAV Serotype 9 |
| Product Type | Adeno-associated virus particles |
| Promoter | CMV |
| Titer | Varies lot by lot, typically ≥1x10^12 GC/mL |
| Size | Varies lot by lot, for example, 30 μL, 50 μL, 100 μL etc. |
| Storage | Store at -80℃. Avoid multiple freeze/thaw cycles. |
| Shipping | Frozen on dry ice |
| Creative Biogene ensures high-quality AAV particles by optimizing and standardizing production protocols and performing stringent quality control (QC). The specific QC experiments performed vary between AAV particle lots. | |
| Endotoxin | Endotoxins, primarily derived from Gram-negative bacteria, can trigger adverse immune responses. Endotoxin contamination is a significant concern in the production of AAV, especially for applications in animal studies and gene therapy. Effective endotoxin quality control is essential in the development and manufacturing of AAV particles. Creative Biogene utilizes rigorous endotoxin detection methods to monitor the endotoxin level in our produced AAV particles to ensure regulatory compliance. |
| Purity | AAV purity is critical for ensuring the safety and efficacy of AAV-based applications.AAV capsids are composed of three main protein components, known as viral proteins: VP1, VP2, and VP3. These proteins play a critical role in the structure and functionality of the AAV capsid. Monitoring the VP1, VP2, and VP3 content in AAV preparations is essential for quality control in AAV production. Our AAV particles are tested for showing three clear bands of VP1, VP2 VP3 by SDS-PAGE. |
| Sterility | The AAV virus samples are inoculated into the cell culture medium for about 5 days to detect bacterial and fungal growth. |
| Transducibility | Upon requirement, Creative Biogene can perform in vitro or in vivo transduction assays to evaluate the ability of AAV to deliver genetic material into target cells or tissues, and assess gene expression and functional activities. |
| Empty vs. Full Capsids | Based-on our proprietary AAV production and purification technology, Creative Biogene can always offer AAV particles with high ratio of full capsids. If required, we can also assess the ratio for a specifc lot of AAV particles by transmission electron microscopy (TEM) or other methods. |
The chemotherapeutic drug doxorubicin is known to induce myofibril damage and cardiac atrophy. Here, researchers tested the potential counteracting effects of the pro-hypertrophic miR-212/132 family on doxorubicin-induced cardiotoxicity. In vitro, overexpression of the pro-hypertrophic miR-212/132 cluster in primary rodent and human iPSC-derived cardiomyocytes suppressed doxorubicin-induced toxicity. Next, a disease model of doxorubicin-induced cardiotoxicity was established in male C57BL/6N mice. Mice were administered adeno-associated virus (AAV)9-control or AAV9-miR-212/132 to achieve myocardial overexpression of the miR-212/132 cluster. AAV9-mediated overexpression limited cardiac atrophy by increasing left ventricular mass and wall thickness, reduced doxorubicin-mediated apoptosis, and prevented myofibril damage. Based on transcriptome analysis, the researchers identified fat storage-induced transmembrane protein 2 (Fitm2) as a novel target and downstream effector molecule, at least in part, responsible for the observed anti-cardiotoxic effects of miR-212/132. Overexpression of Fitm2 partially reversed the effects of miR-212/132. Overexpression of the miR-212/132 family reduced the development of doxorubicin-induced cardiotoxicity and could therefore serve as a therapeutic entry point to limit doxorubicin-mediated adverse cardiac effects.
To assess myofibrillar damage in the study, the researchers analyzed heart sections by transmission electron microscopy. Doxorubicin-induced myofibrillar damage was evident in electron microscopy images of mice that received AAV9 control treatment, manifesting as lower density and damaged myofibrils compared with controls that did not receive doxorubicin (Fig. 1A). Heart sections from animals treated with AAV9-miR-212/132 showed well-preserved myofibrils, indicating that doxorubicin-induced myofibril damage was rescued (Figure 1A). Doxorubicin treatment also induced apoptosis as detected by TUNEL staining (Figures 1B and 1C). The effect of AAV9-miR-212/132 treatment on cardiac cell apoptosis in mice showed only a trend towards reduced apoptosis (Figures 1B and 1C). Doxorubicin treatment also significantly reduced cardiomyocyte size, confirming the atrophy visible on echocardiographic measurements (Figures 1D and 1E). However, treatment with AAV9-miR-212/132 prevented doxorubicin-mediated atrophy and resulted in significant enlargement of cardiomyocytes compared with AAV9 controls that received doxorubicin (Figures 1D and 1E). These results suggest that overexpression of the miR-212/132 cluster abolishes some, but not all, of the cardiotoxic effects of doxorubicin.
Figure 1. AAV9-miR-212/132 Prevents Doxorubicin-Induced Cardiac Apoptosis and Atrophy. (Gupta S K, et al., 2019)
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AAV Serotype 9's consistent performance across different trials has provided us with the baseline we need to evaluate our primary intervention vectors accurately. It’s a dependable standard in our lab’s research.
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