Dr. Zheqing Cai, Founder & CEO, graduated from Beijing University Medical College and worked as a cardiothoracic surgeon in Beijing University Hospital. Dr. Cai obtained his Ph.D. from Medical College of Georgia. Dr. Cai was a NIH-funded investigator and Assistant Professor in Division of Cardiology, Department of Medicine, Johns Hopkins University School of Medicine before starting CL Laboratory.
Frequently asked questions
What is the difference between CL Laboratory and other cardiovascular CRO?
We have extensive documented expertise in cardiovascular research and drug screening, especially in the setting of ischemia-reperfusion injury, post-myocardial infarction remodeling, and diabetic cardiomyopathy. We integrate innovative technology and current knowledge into our approaches, making research productive and outstanding.
What is the advantage of your mouse MI model?
Because we know well about cardiovascular microsurgery, physiology, and anatomy, our expertise minimizes undesired surgical injury and reduces potential study confounders. Mice have high post-MI survival rate, with large infarct size (therapeutic effect is more likely seen). We record electrocardiogram (ECG) during the procedure. Only mice with ST elevation, a reliable indicator of MI, will be included. This prevents experimental variation resulting from non-infarcted mice.
Where do you import animals?
Our rodents are imported directly from AAALAC accredited primary vendors including The Jackson Laboratory, Charles River, Taconic Biosciences, and Envigo.
Where do you perform animal procedures?
Our facility is located within the Science and Technology Park adjacent to the Johns Hopkins East Baltimore campus. All research is conducted in an AAALAC accredited, PHS assured centralized rodent vivarium. Animals are housed in the latest Innovive disposal primary enclosure system on starte-of-art, climate controlled IVC racks. The facility provides top notch biosecurity and employs animal care staff, supervisors, veterinary technicians, and veterinarians with years of experience in biomeical research.
Do you have approved animal protocol for each procedure?
Yes, in compliance with all laws, regulations, accrediting guidelines associated with use of animals in biomedical research, each study we perform is first approved by the facility's Institutional Animal Care and Use Committee (IACUC).
Will you sign non-disclosure agreement before start?
Yes, we will not disclose any information to the third party without your permission.
If I need make 24 mouse models of myocardial infarction, how long will it take to get the work done?
We can purchase mice right after receiving your order. Once we obtain the mice, we will make 8 models a day. The entire process may take two weeks from making a request to receiving infarcted mice.
What happens if mice die during procedure?
We purchase additional 10% of the requested rodents, with no added charge to you. Your target sample size will therefore never be affected by mortalities occuring during the induction phase.
Peer Reviewed Publications (*: corresponding author)
Cai ZP, Luo W, Zhan H, Semenza GL. Hypoxia-inducible factor 1 is required for remote ischemic preconditioning of the heart. Proc Natl Acad Sci U S A. 2013;110:17462-7.
Cai ZP*, Parajuli N, Zheng X, Becker L. Remote ischemic preconditioning confers late protection against myocardial ischemia-reperfusion injury in mice by upregulating interleukin-10. Basic Res Cardiol. 2012;107:277.
Sarkar K, Cai Z, Gupta R, Parajuli N, Fox-Talbot K, Darshan MS, Gonzalez FJ, Semenza GL. Hypoxia-inducible factor 1 transcriptional activity in endothelial cells is required for acute phase cardioprotection induced by ischemic preconditioning. Proc Natl Acad Sci U S A. 2012;109:10504-9.
Parajuli N, Yuan Y, Zheng X, Bedja D, Cai ZP*. Phosphatase PTEN is critically involved in post-myocardial infarction remodeling through the Akt/interleukin-10 signaling pathway. Basic Res Cardiol. 2012;107:248.
Zu L, Zheng X, Wang B, Parajuli N, Steenbergen C, Becker LC, Cai ZP*. Ischemic preconditioning attenuates mitochondrial localization of PTEN induced by ischemia-reperfusion. Am J Physiol. 2011;300:H2177-86.
Zu L, Shen Z, Wesley J, Cai ZP*. PTEN inhibitors cause a negative inotropic and chronotropic effect in mice. Eur J Pharmacol. 2011;650:298-302.
Zu L, Bedja D, Fox-Talbot K, Gabrielson KL, Van Kaer L, Becker LC, Cai ZP*. Evidence for a role of immunoproteasomes in regulating cardiac muscle mass in diabetic mice. J Mol Cell Cardiol. 2010;49:5-15.
Cai ZP*, Shen Z, Van Kaer L, Becker LC. Ischemic preconditioning-induced cardioprotection is lost in mice with immunoproteasome subunit LMP-2 deficiency. FASEB J. 2008;22:4248-57.
Cai Z, Zhong H, Bosch-Marce M, Fox-Talbot K, Wang L, Wei C, Trush MA, Semenza GL. Complete loss of ischaemic preconditioning-induced cardioprotection in mice with partial deficiency of HIF-1 alpha. Cardiovasc Res.2008;77:463-70.
Sullivan JC, Goodchild TT, Cai Z, Pollock DM, Pollock JS. ETA and ETB receptor mediated regulation of NOS1 and NOS3 isoforms in the renal inner medulla. Acta Physiol. 2007;191:329-36.
Yang XP, Mattagajasingh S, Su S, Chen G,Cai Z, Fox-Talbot K, Irani K, Becker LC. Fractalkine upregulates intercellular adhesion molecule-1 in endothelial cells through CX3CR1 and the Jak-Stat5 pathway. Circ Res. 2007;101:1001-8.
Cai Z*, Semenza GL. PTEN activity is modulated during ischemia and reperfusion: involvement in the induction and decay of preconditioning. Circ. Res. 2005;97:1351-9.
Cai Z, Semenza GL. Phosphatidylinositol-3-kinase signaling is required for erythropoietin-mediated acute protection against myocardial ischemia/reperfusion injury. Circulation. 2004;109:2050-3.
Kelly BD, Hackett SF, Hirota K, Oshima Y,Cai Z, Berg-Dixon S, Rowan A, Yan Z, Campochiaro PA, Semenza GL. Cell type-specific regulation of angiogenic growth factor gene expression and induction of angiogenesis in nonischemic tissue by a constitutively active form of hypoxia-inducible factor 1. Circ. Res. 2003;93:1074-81.
Cai Z, Manalo DJ, Wei G, Rodriguez ER, Fox-Talbot K, Lu H, Zweier JL, Semenza GL. Hearts from rodents exposed to intermittent hypoxia or erythropoietin are protected against ischemia-reperfusion injury. Circulation. 2003:108:79-85.
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