- Cardiovascular Physiological Phenomena
- Cell Communication
- Cell Physiological Phenomena
- Molecular Biology
- Paracrine Communication
- Physiological Genomics
- Renal Physiology
Methodologies and Techniques
- miRNA analysis
- Models of Cardiac Pathology
- Models of Renal Pathology
- Next-generation RNA Sequencing
- RNA analysis
- Rodent Echocardiography
- Rodent Left Ventricle Pressure-Volume Loop Analysis
- Western Blot
Cardiovascular Physiology | Genetics and Genomics | Molecular and Cellular Physiology | Renal Physiology
Our research is broadly centered on understanding how alterations in microRNAs and protein coding genes influence cardiovascular disease, renal disease, and cardiorenal syndromes. Cardiorenal syndromes are a grouping of human clinical conditions where primary disease in either the heart or the kidney contributes to the development of secondary disease in the other organ.
Our current focus is on cardiorenal syndrome type 4 (CRS4), also known as chronic renocardiac syndrome, a condition in which chronic kidney disease (CKD) contributes to the development of cardiovascular diseases including hypertrophy, diastolic dysfunction, reduction in cardiac function and increased risk of cardiovascular events.
CRS4 is clinical problem that has received a great deal of attention in recent years because of the large number of people impacted and the high associated healthcare costs. In 2010 the Centers for Disease Control estimated that more than 10% of adults in the United States population chronic kidney disease, and cardiovascular pathology is leading cause of death in these patients. Treatment of CRS4 remains challenging because so little is understood about the pathology of the disease. Adult patients with CKD often have age associated comorbidities, such as diabetes, hypertension, and atherosclerosis, making it difficult to identifying mediators of the pathology in this population.
Our goals are focused on identifying the essential components of cardiorenal syndromes and their therapeutic targets. We have started to investigate the molecular mediators of this conditions using a 5/6 nephrectomy (5/6 NX) model of CKD in Sprague Dawley rats. This model of CKD allows us to study CRS4 related pathologies in the absence of confounding comorbidities that would independently impact the heart, such as atherosclerosis, diabetes and hypertension.
Our current goals in CRS4 research interest include:
We combine in vivo approaches for studying cardiac and renal function with advanced molecular techniques to comprehensively study the factors that influence left ventricular pathology. Frequently utilized techniques in our laboratory include: echocardiography, left ventricle pressure-volume relationship analysis, chronic and acute blood pressure recordings, cell culture models (siRNA, miRNA), in vitro and in vivo miRNA suppression, immunohistochemistry, in situ hybridization, western blot analysis, ELISA, miRNA and mRNA next generation sequencing and qRT-PCR.
Research for this project is supported an American Heart Association Scientist Development Grant (13SDG17100095).
Supplemental Table 1 (XLSX)
Supplemental Table 3 (XLSX)
Supplemental Table 4 (XLSX)
Students with an interest in this research are encouraged to contact Dr. Kriegel at firstname.lastname@example.org.
(Paterson MR, Geurts AM, Kriegel AJ.) Kidney Int. 2019 Dec;96(6):1332-1345 PMID: 31668631 PMCID: PMC6941490 SCOPUS ID: 2-s2.0-85074541202 11/02/2019
(Abais-Battad JM, Alsheikh AJ, Pan X, Fehrenbach DJ, Dasinger JH, Lund H, Roberts ML, Kriegel AJ, Cowley AW Jr, Kidambi S, Kotchen TA, Liu P, Liang M, Mattson DL.) Hypertension. 2019 10;74(4):854-863 PMID: 31476910 PMCID: PMC6739138 SCOPUS ID: 2-s2.0-85072134357 09/04/2019
(Hader SN, Zinkevich N, Norwood Toro LE, Kriegel AJ, Kong A, Freed JK, Gutterman DD, Beyer AM.) Am J Physiol Heart Circ Physiol. 2019 10 01;317(4):H705-H710 PMID: 31397169 PMCID: PMC6843017 SCOPUS ID: 2-s2.0-85072508643 08/10/2019
(Lai PY, Jing X, Michalkiewicz T, Entringer B, Ke X, Majnik A, Kriegel AJ, Liu P, Lane RH, Konduri GG.) Physiol Genomics. 2019 09 01;51(9):462-470 PMID: 31373541 PMCID: PMC6766700 SCOPUS ID: 2-s2.0-85072265843 08/03/2019
(Nasci VL, Chuppa S, Griswold L, Goodreau KA, Dash RK, Kriegel AJ.) Am J Physiol Heart Circ Physiol. 2019 03 01;316(3):H710-H721 PMID: 30657727 PMCID: PMC6459316 SCOPUS ID: 2-s2.0-85062599405 01/19/2019
(Ilatovskaya DV, Levchenko V, Pavlov TS, Isaeva E, Klemens CA, Johnson J, Liu P, Kriegel AJ, Staruschenko A.) EBioMedicine. 2019 Feb;40:663-674 PMID: 30745171 PMCID: PMC6413684 SCOPUS ID: 2-s2.0-85061112508 02/13/2019
(Baker MA, Wang F, Liu Y, Kriegel AJ, Geurts AM, Usa K, Xue H, Wang D, Kong Y, Liang M.) Hypertension. 2019 02;73(2):399-406 PMID: 30595117 PMCID: PMC6339564 SCOPUS ID: 2-s2.0-85059796489 01/01/2019
(Liu Y, Kriegel AJ, Liang M.) Methods Mol Biol. 2019;2018:177-194 PMID: 31228157 SCOPUS ID: 2-s2.0-85068180336 06/23/2019
(Miller JJ, Aoki K, Mascari CA, Beltrame AK, Sokumbi O, North PE, Tiemeyer M, Kriegel AJ, Dahms NM.) FASEB J. 2019 01;33(1):418-429 PMID: 29979634 PMCID: PMC6629127 SCOPUS ID: 2-s2.0-85059237456 07/07/2018
(Kriegel AJ, Terhune SS, Greene AS, Noon KR, Pereckas MS, Liang M.) J Biol Chem. 2018 09 07;293(36):14080-14088 PMID: 30006350 PMCID: PMC6130969 SCOPUS ID: 2-s2.0-85053013199 07/15/2018
(Widlansky ME, Jensen DM, Wang J, Liu Y, Geurts AM, Kriegel AJ, Liu P, Ying R, Zhang G, Casati M, Chu C, Malik M, Branum A, Tanner MJ, Tyagi S, Usa K, Liang M.) EMBO Mol Med. 2018 03;10(3) PMID: 29374012 PMCID: PMC5840545 SCOPUS ID: 2-s2.0-85041063208 01/28/2018
(Chuppa S, Liang M, Liu P, Liu Y, Casati MC, Cowley AW, Patullo L, Kriegel AJ.) Kidney Int. 2018 02;93(2):375-389 PMID: 28760335 PMCID: PMC5787401 SCOPUS ID: 2-s2.0-85026463717 08/02/2017