Developmental Cellular Physiology and Pathophysiology Lab
- Function of the Wilms tumor protein WT1 in embryonic development and disease
- Molecular mechanisms of oxygen-dependent gene expression
- Developmental erythropoietin production in liver and kidney
- Role of polyamines in acute and chronic kidney injury
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Main research topics of the Developmental Cellular Physiology and Pathophysiology Lab
Our group is interested in transcriptional mechanisms controlling cardiovascular development and formation of the genitourinary system. The major focus of our work is on the regulation and function of the Wilms’ tumor gene, WT1. Another research topic is the regulation of gene expression by the local oxygen concentration and hypoxia, respectively.
Amine Oxidase Copper-containing 1 (AOC1) in renoprotection
Polyamines are low molecular weight organic polycations that regulate various processes involved in tissue injury and repair, such as gene expression, cell proliferation and autophagy. The synthesis, interconversion and degradation of polyamines are enzymatically regulated. Within the CRC 1365 “Renoprotection” (project B05), we investigate the role of the polyamine system in kidney injury. Our preliminary data show increased expression of polyamine synthesizing enzymes and reduced levels of polyamine degrading enzymes in various experimental kidney pathologies due to ischemia-reperfusion, transplantation and treatment with cyclosporin A, among others. Strikingly, damaged kidneys display de novo expression of the putrescine degrading enzyme amine oxidase copper-containing 1 (AOC1) in proximal tubules. Aoc1 expression closely correlates with the severity of kidney injury and is up-regulated also in patient allografts after transplantation. Furthermore, tonicity-induced transcription of NFAT5 (nuclear factor of activated T cells-5), which is enhanced upon kidney damage, stimulates Aoc1 expression in cultured kidney cells. Overexpression of AOC1 promotes autophagy, i.e. the removal of unnecessary or dysfunctional components, in kidney cells in vitro.
We currently investigate the hypothesis that impaired polyamine metabolism underlies several kidney injury forms, thus, being a potential target for renoprotection. To this end, we have generated two mouse lines with Aoc1 knockout, one exhibiting germline deletion of Aoc1, and the other one displaying conditional Aoc1 knockout in proximal kidney tubules. As healthy mouse kidneys lack AOC1, we see no overt kidney phenotype in these mice. Aoc1 knockout mice will be exposed to renal ischemia-reperfusion and oxalate-induced kidney injury followed by in-depth characterization. Genetic and clinical testing of a family with heterozygous AOC1 deletion and end-stage renal disease will translate our findings. Mechanistically, we will investigate the role of AOC1 in the cellular stress response and its influence on renal cell metabolism. CRISPR/Cas9 library screening with kidney cells will decipher underlying regulatory pathways and further assess AOC1 for prospective application in renoprotection.
Sieckmann T, Kirschner KM: Polyamines, metabolites and metabolomics. Acta Physiol (Oxf.) 229(3): e13480, 2020.
Function and regulation of Wilms tumor protein WT1
The transcription factor WT1 was initially identified as a suppressor of pediatric kidney cnacer (Wilms tumor, nephroblastoma). Wilms tumors develop when normal kidney development goes wrong due to a failure of nephron differentiation from the metanephric mesenchyme. Wt1 knockout mice lack kidneys and gonads and are embryonic lethal. Other developmental abnormalities of Wt1-deficient mice pertain to the coronary vasculature, sensory neuroepithelia and the hematopoietic system. Experimental data support the view that WT1 enables a reciprocal switch between a mesenchymal and epithelial cellular state in these tissues. Conditional Wt1 inactivation in adult mice causes multiple organ failure including glomerulosclerosis of the kidney, abnormal hematopoiesis as well as loss of bone and fat mass. These observations indicate that WT1 function is not restricted to embryonic development, but required for tissue homeostasis throughout adulthood.
We investigate the role of WT1 in development and disease by identifying WT1 target genes in various tissues. As such, we discovered that WT1 activates transcription of the erythropoietin (EPO) and EPO receptor genes. Other WT1 targets include Kdr and Ntrk2 encoding VEGF receptor 2 and neurotrophin receptor TrkB, respectively. Furthermore, WT1 is a transcriptional activator of amine oxidase copper-containing 1 (AOC1), the enzyme catalyzing polyamine breakdown. Polyamines play an important role in kidney development. Our recent findings indicate that impaired polyamine metabolism is a hallmark of various types of kidney injury.
Kirschner KM, Sciesielski LK, Krueger K, Scholz H: Wilms tumor protein-dependent transcription of VEGF receptor 2 and hypoxia regulate expression of the testis-promoting gene Sox9 in murine embryonic gonads. J Biol Chem 292: 20281-20291, 2017.
Kirschner KM, Braun JF, Jacobi CL, Rudigier LJ, Persson AB, Scholz H: Amine oxidase copper-containing 1 (AOC1) is a downstream target gene of the Wilms tumor protein, WT1, during kidney development. J Biol Chem 289: 24452-24462, 2014.
Dame C, Kirschner KM, Bartz KV, Wallach T, Hussels CS, Scholz H: Wilms’ tumor suppressor, Wt1, is a transcriptional activator of the erythropoietin gene. Blood 107: 4282-4290, 2006
Wagner N, Wagner KD, Hammes A, Kirschner KM, Vida, VP, Schedl A, Scholz H: A splice variant of the Wilms’ tumour suppressor Wt1 is required for normal development of the olfactory system. Development 132: 1327-1336, 2005.
Wagner N, Wagner KD, Theres H, Englert C, Schedl A, Scholz H: Coronary vessel development requires activation of the TrkB neurotrophin receptor by the Wilms' tumor transcription factor Wt1. Genes Dev. 19(21): 2631-2642, 2005.
Wagner KD, Wagner N, Vidal VP, Schley G, Wilhelm D, Schedl A, Englert C, Scholz H: The Wilms’ tumor gene Wt1 is required for normal development of the retina. EMBO J 21: 1398-1405, 2002.
Molecular mechanisms of oxygen-dependent gene expression
Regulation of gene expression by oxygen is essential for normal development. Furthermore, insufficient oxygenation (hypoxia) may cause severe tissue injury and promote tumor growth. Hypoxia-inducible factors (HIFs) are master regulators of gene expression in hypoxic cells. The HIF family of basic helix-loop-helix transcription factors comprises three members, each one composed of a variable, oxygen-sensitive α-subunit (HIF-1α/ 2α /3α) and a constitutive β-subunit (ARNT, Aryl Hydrocarbon Receptor Nuclear Translocator). In a project funded by the Wilhelm-Sander-Stiftung (Project-No. 2018.015.2), we could show that HIF-2 stimulates WT1 expression in neuroblastoma cells by interacting with an intronic enhancer in the WT1 gene. Neuroblastoma is a malignant childhood tumor originating from embryonic neural crest cells. Neuroblastoma accounts for approximately 8% of pediatric malignancies and is the most prevalent extracranial tumor in children. High levels of HIF-2 due to tumor hypoxia correlate with poor prognosis. Our data suggest that HIF-2-mediated stimulation of WT1 expression influences the progression of neuroblastoma.
We set out to identify target genes of WT1 and HIFs in neuroblastoma. For this purpose, we use CRISPR/Cas9 genome editing to inactivate these factors in neuroblastoma cells. Tumor cells with and without WT1/ HIFs are exposed in hypoxia (1% O2), and their transcriptome is determined by next generation sequencing. Chromatin immunoprecipitation (ChIP) sequencing is used to map genomic binding sites of WT1 and HIFs in hypoxic neuroblastoma cells. We expect to obtain novel insights into oxygen-dependent control of gene expression in neuroblastoma. Ideally, this can pave the way toward novel therapeutic strategies.
Krueger K, Catanese L, Sciesielski LK, Kirschner KM, Scholz H: Deletion of an intronic HIF-2α binding site suppresses hypoxia-induced WT1 expression. Biochim Biophys Acta Gene Regul Mech 1862: 71-83, 2019.
Martens LK, Kirschner KM, Warnecke C, Scholz H: Hypoxia-inducible factor-1 (HIF-1) is a transcriptional activator of the TrkB neurotrophin receptor gene. J Biol Chem 282: 14379-14388, 2007.
Wagner KD, Wagner N, Wellmann S, Schley G, Bondke A, Theres H, Scholz H: Oxygen-regulated expression of the Wilms’ tumor suppressor Wt1 involves hypoxia-inducible factor-1 (HIF-1). FASEB J 17(10): 1364-1366, 2003.
Transcriptional control of visceral white adipose tissue
Two types of adipose tissue can be discerned: (i) Subcutaneous and visceral (intra-abdominal) white adipose tissue (WAT) serving mainly for energy storage. (ii) Brown adipose tissue (BAT), which fuels energy expenditure by non-shivering thermogenesis. This process involves uncoupling protein 1 (UCP1), a pore-forming molecule in the inner mitochondrial membrane, which dissociates proton influx from ATP-synthesis. Unlike subcutaneous WAT, which is protective, visceral fat accumulation correlates with chronic disease including diabetes, arterial hypertension, metabolic syndrome and cancer. Visceral and subcutaneous WAT also differ in their browning capacity. Browning describes the appearance of thermogenic beige/ brite (brown-in-white) adipocytes in classical WAT under favorable conditions such as chronic cold exposure and β-adrenergic stimulation. Beige adipocytes display characteristics of both, white and brown fat cells. WAT browning has recently attracted broad attention for its potential application to reduce excessive body weight and combat metabolic disease.
We recently discovered that heterozygous Wt1 knockout mice – unlike their wild-type littermates – show morphological and molecular signs of browning including up-regulation of thermogenic genes (Ucp1, Cpt1b) in their visceral WAT. Importantly, WT1 expression is normally restricted to preadipocytes in visceral fat. WT1 is not detected in mature adipocytes in visceral WAT and is absent from subcutaneous fat and interscapular BAT of mice. Our findings on heterozygous Wt1 knockout mice suggest that WT1 suppresses a brown cell fate in visceral WAT. Accordingly, WT1 overexpression down-regulated thermogenic genes (Ucp1, Ppargc1a, Prdm16, Cidea) in differentiating brown preadipocytes in vitro. Interestingly, heterozygous Wt1 knockout mice are protected, at least partially, against high-fat diet-induced hepatic steatosis and glucose intolerance. We assume that improved metabolic health is due to expression of UCP1 and other thermogenic molecules in their visceral WAT.
To test this hypothesis, we will generate mice with conditional Wt1 inactivation in visceral fat. These mice and their wild-type littermates will be characterized under baseline conditions and metabolic stress caused by high-fat diet, cold exposure and β-adrenergic stimulation. Readout parameters include WAT browning, glucose homeostasis and lipid metabolism. Additionally, we will identify WT1 target genes in visceral preadipocytes using RNA- and ChIP-sequencing technology.
Kirschner KM, Foryst-Ludwig A, Gohlke S., Li C, Flores RE, Kintscher U, Schupp M, Schulz TJ, Scholz H: Wt1 haploinsufficiency induces browning of epididymal fat and alleviates metabolic dysfunction in mice on high-fat diet. Diabetologia 65(3): 528-540, 2022.
Kirschner KM, Scholz H: WT1 in adipose tissue: from development to adult physiology. Front Cell Dev Biology 10: 854120. doi: 10.3389/fcell, 2022.
German Research Foundation: DFG CRC 1365 Renoprotection, B05 Amine oxidase copper-containing-1 enzyme in renoprotection, Project leader: Dr. Karin Kirschner, Professor Dr. Holger Scholz, 2023.
Wilhelm Sander-Stiftung Project 2018.015.2: Characterization of WT1 as a potential target molecule in neuroblastomen, Project leader: Professor Dr. Holger Scholz, 2021-2022.
German Research Foundation: DFG CRC 1365 Renoprotection, B05 The polyamine system in gender-related renoprotection, Project leader: Dr. Karin Kirschner, Professor Dr. Holger Scholz, 2019-2022.
Wilhelm Sander-Stiftung Project 2018.015.1: Characterization of WT1 as a potential target molecule in neuroblastomen, Project leader: Professor Dr. Holger Scholz, 2018-2020.
Deutsche Diabetes Stiftung: FB-0403-2017: Impact of the Wt1 genotype on glucose homeostasis, Project leader: Professor Dr. Holger Scholz, 2018-2019.
German Research Foundation: DFG KI 1441/4-1: Molecular mechanisms of adaptation to intrauterine and perinatal changes of oxygen partial pressure: The liver-to-kidney switch of Erythropoietin production as model System, Project leader: Dr. Karin Kirschner, 2017-2020.
Else Kröner-Fresenius-Stiftung: 2014_A23: The Wilms tumor protein Wt1 and diabetes mellitus, Project leader: Professor Dr. Holger Scholz, 2014-2017
German Research Foundation: DFG SCHO 634/8-1: Regulation and synergism of transcription factors Wt1 and Gata 4 in the heart and gonads, Project leader: Professor Dr. Holger Scholz, 2011-2014.
German Research Foundation: DFG SCHO 634/6-1: Mechanisms and consequences of an oxygen-dependent expression of TrkB neurotrophin receptor, Project leader: Professor Dr. Holger Scholz, 2007-2010.
German Research Foundation: DFG FA 845/2-2: Posttranscriptional control of bHLH transcription factor Mash1 gene expression rate, in co-operation with Prof. Dr. Michael Fähling, 2008-2014.
Prof. Dr. Christof Dame/ Dr. Lina Sciesielski (Molekulare Neonatologie, Charité)
Prof. Dr. Christoph Englert (Fritz-Lipmann-Institut, Jena)
Prof. Dr. Christian Freund (Institut für Biochemie, Freie Universität Berlin)
Prof. Dr. Jan Halbritter (Medizinische Klinik mit Schwerpunkt Nephrologie, Charité)
Prof. Dr. Ulrich Kintscher (Institut für Pharmakologie, Charité)
Prof. Dr. Dominik Müller (Max-Delbrück-Centrum für Molekulare Medizin, Berlin)
Prof. Dr. Ralf Mrowka (Experimentelle Nephrologie, Universitätsklinikum Jena)
PD Dr. Gunnar Schley (Medizinische Klinik IV, Universitätsklinikum Erlangen)
Prof. Dr. Kai Schmidt-Ott (Klinik für Nephrologie, Medizinische Hochschule Hannover)
Prof. Dr. Tim Schulz, Deutsches Institut für Ernährungsforschung, Potsdam-Rehbrücke
Prof. Dr. Michael Schupp, Institut für Pharmakologie, Charité Berlin
Prof. Dr. Roland Wenger (Physiologisches Institut, Universität Zürich, Schweiz)
Publications (since 2010)
Zinzius K, Marchetti GM, Fischer R, Milrad Y, Oltmanns A, Kelterborn S, Yacoby I, Hegemann P, Scholz M, Hippler M: Calredoxin regulates the chloroplast NADPH-dependent thioredoxin reductase in Chlamydomonas reinhardtii. Plant Physiology 00:1-19, 2023
Catalan RE, Fragkopoulos AA, von Trott N, Kelterborn S, Baidukova O, Hegemann P, Bäumchen O: Light-regulated adsorption and desorption of Chlamydomonas cells at surfaces. Soft Matters 19:306-314, 2023
Sieckmann T, Schley G, Ögel N, Kelterborn S, Boivin F, Fähling M, Ashraf MI, Reichel M, Vigolo E, Hartner A, Lichtenberger F-B, Breiderhoff T, Knauf F, Rosenberger C, Aigner F, Schmidt-Ott K, Scholz H, Kirschner KM: Strikingly conserved gene expression changes of polyamine regulating enzyme among various forms of acute and chronic kidney injury. Kidney International 104:90-107, 2023
Klämbt V, Buerger F, Wang C, Naeret T, Richter K, Nauth T, Weiss A-C, Sieckmann T, Lai E, Connaughton DM, Seltzsam S, Mann N, Majmundar AJ, Wu C-HW, Onuchic-Whitford AC, Shril S, Schneider S, Schierbaum L, Dai R, Bekheirnia MR, Joosten M, Shlomovitz O, Vivante A, Banne E, Mane S, Lifton RP, Kirschner KM, Kispert A, Rosenberger G, Fischer K-D, Lienkamp SS, Zegers MMP, Hildebrandt F:
Genetic variants in ARHGEF6 cause congenital anomalies of the kidney and urinary tract in humans, mice, and frogs. Journal of the American Society of Nephrology/JASN 34:273-290, 2023
Baidukova O, Oppermann J, Kelterborn S, Fernandez Lahore RG, Schumacher D, Evers H, Kamrani YY, Hegemann P: Gating and ion selectivity of Channelrho-dopsins are critical for photo-activated orientation of Chlamydomonas as shown by in vivo point mutation. Nature communications 13:7253, 2022
Kirschner KM: Open research data - Expectations and limitations. Acta Physiologica 236:e13900, 2022
Neusius D, Kleinknecht L, Teh JT, Ostermeier M, Kelterborn S, Eirich J, Hegemann P, Finkemeier I, Bohne AV, Nickelsen J: Lysine acetylation regulates moonlighting activity of the E2 subunit of the chloroplast pyruvate dehydrogenase complex in Chlamydomonas. Plant J. 111(6):1780-1800, 2022
Yilmaz DE, Kirschner K, Demirci H, Himmerkus N, Bachmann S, Mutig K: Immunosuppressive calcineurin inhibitor cyclosporine A induces pro-apoptotic endoplasmic reticulum stress in renal tubular cells. J Biol Chem. 298:101589, 2022
Scholz H: Erythropoietin – producing cells in the kidney: Novel insights in their long-term fate during hypoxaemia and renal tissue remodeling. Acta Physiologica 234:e13786, 2022
Kirschner KM, Foryst-Ludwig A, Gohlke S, Li C, Flores RE, Kintscher U, Schupp M, Schulz TJ, Scholz H: Wt1 haploinsufficiency induces browning of epididymal fat and alleviates metabolic dysfunction in mice on high-fat diet. Diabetologia 65:528-540, 2022
Sciesielski LK, Felten M, Michalick L, Kirschner KM, Lattanzi G, Jacobi CLJ, Wallach T, Lang V, Landgraf D, Kramer A, Dame C: The circadian clock regulates rhythmic erythropoietin expression in the murine kidney. Kidney Int. 100:1071-1080, 2021
Kirschner KM: Reduce, replace, refine – Animal experiments. Acta Physiologica 233:e13726, 2021
Schmidt V, Sieckmann T, Kirschner KM, Scholz H: WT1 regulates HOXB9 gene expression in a bidirectional way. BBA – Gene Regulatory Mechanisms 1864(11-12):194764, 2021
Scholz H, Boivin FJ, Schmidt-Ott KM, Bachmann S, Eckardt KU, Scholl UI, Persson PB: Kidney physiology and susceptibility to acute kidney injury: implications for renoprotection. Nature Reviews/Nephrology 17: 335-349, 2021
Sizova I, Kelterborn S, Verbenko V, Kateriya S, Hegemann P: Chlamydomonas POLQ is necessary for CRISPR/Cas9-mediated gene targeting. G3 (Bethesda). 11(7):jkab114, 2021
Xu N, Oltmanns A, Zhao L, Girot A, Karimi M, Hoepfner L, Kelterborn S, Scholz M, Beißel J, Hegemann P, Bäumchen O, Liu LN, Huang K, Hippler M: Altered N-glycan composition impacts flagella-mediated adhesion in Clamydomonas reinhardtii. eLife 9:e58805, 2020
Münch J, Kirschner KM, Schlee H, Kraus C, Schönauer R, Jin WJ, Le Duc D, Scholz H, Halbritter J: Autosomal dominant polycystic kidney disease in absence of renal cyst formation illustrates genetic interaction between WT1 and PKD1. J Med Genet 0:1-5, 2020
Sieckmann T, Kirschner KM: Polyamines, metabolites and metabolomics. Acta Physiologica 230:e13480, 2020
Sciesielski LK, Kirschner KM: HIF prolyl hydroxylase inhibitors – the new lifestyle drug? Acta Physiologica 227: e13370, 2019
Krueger K, Catanese L, Scholz H: Intermittent hypoxia: Friend and foe. Acta Physiologica 226:e13276, 2019
Krueger K, Catanese L, Sciesielski LK, Kirschner KM, Scholz H: Deletion of an intronic HIF-2α binding site suppresses hypoxia-induced WT1 expression. Biochemica et Biophysic Acta, BBA – Gene Regulatory Mechanisms: 1862:71-83, 2019
Schmidt V, Kirschner KM: Alternative pre-mRNA splicing. Acta Physiologica 222:e13053, 2018
Mathia S, Rudigier LJ, Kasim M, Kirschner KM, Persson PB, Eckardt K-U, Rosenberger C, Fähling M: A dual role of miR-22 in rhabdomyolysis-induced acute kidney injury. Acta Physiologica 224: e13102, 2018
Greiner A, Kelterborn S, Evers H, Kreimer G, Sizova I, Hegemann P: Targeting of Photoreceptor Genes in Chlamydomonas reinhardtii via Zinc-Finger Nucleases and CRISPR/Cas9. Plant Cell 29:2498-2518, 2017
Kirschner KM, Sciesielski LK, Krueger K, Scholz H: Wilms tumor protein-dependent transcription of VEGF receptor 2 and hypoxia regulate expression of the testis-promoting gene Sox9 in murine embryonic gonads. Journal of Biological Chemistry 292: 20281-2091, 2017
Müller M, Bondke Persson A, Krueger K, Kirschner KM, Scholz H: The Wilms tumor protein WT1 stimulates transcription of the gene encoding insulin-like growth factor binding protein 5 (IGFBP5). Gene 619: 21-29, 2017
Rudigier LJ, Dame C, Scholz H, Kirschner KM: Ex vivo cultures combined with vivo-morpholino induced gene knockdown provide a system to assess the role of WT1 and GATA4 during gonad Differentiation. PLOS one 12: e0176296, 2017
Kasim, M, Heß V, Scholz H, Persson PB, Fähling M: Achaete-Scute Homolog 1 Expression Controls Cellular Differentiation of Neuroblastoma. Frontiers in Molecular Neuroscience 9:156, 2016
Krueger K, Shen J, Maier A, Tepel M, Scholze A: Lower Superoxide dismutase 2 (SOD2) Protein Content in mononuclear cells is associated with better survival in patients with hemodialysis therapy. Oxidative Medicine and Cellular Longevity, Volume 2016. Article ID 7423249, 8 pages, 2016
Holzweber M, Lippitz A, Krueger K, Jankowski J, Unger WES: Surface characterization of dialyzer polymer membranes by Imaging ToF-SIMS and quantitative XPS line scans. Biointerphases 10: 019011, 2015
Persson PB, Müller M: Transcription. Acta Physiologica 215: 159-160, 2015
Schley G, Scholz H, Kraus A, Hackenbeck T, Klanke B, Willam C, Wiesener MS, Heinze E, Burzlaff N, Eckardt K-U, Buchholz B: Hypoxia inhibits nephrogenesis through paracrine Vegfa despite the ability to enhance tubulogenesis. Kidney Intern., 88: 1283-1292, 2015
Albert GI, Schell C, Kirschner KM, Schäfer S, Naumann R, Müller A, Kretz O, Kuropka B, Girbig M, Hübner N, Krause E, Scholz H, Huber TB, Knobeloch K-P, Freund C: The GYF Domain Protein CD2BP2 is critical for embryogenesis and podocyte function. J Mol Cell Biol, 7: 402-414, 2015
Staudacher JJ, Naarmann-de Vries IS, Ujvari SJ, Klinger B, Kasim M, Benko E, Ostareck-Lederer A, Ostareck DH, Bondke Persson A, Lorenzen S, Meier JC, Blüthgen N, Persson PB, Henrion-Caude A, Mrowka R, Fähling M: Hypoxia-induced gene expression results from selective mRNA partitioning to the endoplasmic reticulum. Nucleic Acids Research, 43: 3219-3236, 2015
Kirschner KM, Braun JFW; Jacobi CL, Rudigier LJ, Bondke Persson A, Scholz H: Amine Oxidase Copper-containing 1 (AOC1) Is a Downstream Target Gene of the Wilms Tumor Protein, WT1, during Kidney Development. Journal of Biological Chemistry 289: 24452-24462, 2014
Jacobi CLJ, Rudigier LJ, Scholz H, Kirschner KM: Transcriptional regulation by the Wilms tumor protein, Wt1, suggests a role of the metalloproteinase Adamts16 in murine genitourinary development. Journal of Biological Chemistry 289(16): 11566, 2014 (Additions and Corrections)Dülsner A, Gatzke N, Hillmeister P, Glaser J, Zietzer A, Nagorka S, Janke D, Pfitzner J, Stawowy P, Meyborg H, Urban D, Bondke Persson A, Buschmann IR: PPARγ activation inhibits cerebral arteriogenesis in the hypoperfused rat brain. Acta Physiologica, 210: 354-368, 2014
Bondke Persson A and Persson PB: Sleep. Acta Physiologica 210: 229-230, 2014
Bondke Persson A and Persson PB: Dealing with radicals. Acta Physiologica 210: 2-4, 2014
Radeck J, Kraft K, Bartels J, Cikovic T, Dürr F, Emenegger J, Kelterborn S, Sauer C, Fritz G, Gebhard S, Mascher T: The Bacillus BioBrick Box: generation and evaluation of essential genetic building blocks for standardized work with Bacillus subtilis. J Biol Eng. 7:29, 2013
Bondke Persson, A and Persson, PB: The physiologist: researcher, inventor, physician, educator and visionary. Acta Physiologica 209: 193-194, 2013
Bondke Persson A: G – protein – receptors, signals and function. Acta Physiol 209: 91-93, 2013
Bondke Persson A, Persson PB: Tools of our trade. Acta Physiol 208: 289-291, 2013
Bondke Persson A, Persson PB: On beauty. Acta Physiol 208: 215- 217, 2013
Duelsner A, Bondke Persson A: Animal models in cardiovascular research. Acta Physiol 208: 1- 5, 2013
Persson PB, Bondke Persson A: Nitric oxide: a classic revisited. Acta Physiologica 207: 427-429, 2013
Persson PB, Bondke Persson A: A matter of taste. Acta Physiologica 207: 203-205, 2013
Persson PB, Bondke Persson A: Obesity: The BIG issue. Acta Physiologica 207: 1-4, 2013
Jacobi CLJ, Rudigier LJ, Scholz H, Kirschner KM: Transcriptional regulation by the wilms tumor protein, Wt1, suggests a role of the metalloproteinase Adamts16 in murine genitourinary development. The Journal of Biol Chem 288(26): 18811-18824, 2013
Fähling M, Persson AB, Klinger B, Benko E, Steege A, Kasim M, Patzak A, Persson PB, Wolf G, Blüthgen N, Mrowka R: Multi-level regulation of HIF-1 signaling by TTP. Mol Biol Cell 23:4129-4141, 2012
Bondke Persson A and Persson, PB: Cycling in Physiology. Acta Physiologica (Oxford) 206: 1-3, 2012
Dülsner A, Gatzke N, Glasner J, Hillmeister P, Li M, Lee EJ, Lehmann K, Urban D, Meyborg H, Stawowy P, Busjahn A, Nagorka S, Bondke Persson A, Buschmann IR: Acetylsalicylic acid, but no clopidogrel, inhibits therapeutically induced cerebral arteriogenesis in the hypoperfused rat brain. J Cerebral Blood Flow & Metabolism 32: 105-114, 2012
Dülsner A, Gatzke N, Glaser J, Hillmeister P, Li M, Lee EJ, Lehmann K, Urban D, Meyborg H, Stawowy P, Busjahn A, Nagorka S, Bondke Persson A, Buschmann IR: Granulocyte Colony-Stimulating Factor Improves Cerebrovascular Reserve Capacity by Enhancing Collateral Growth in the Circle of Willis. Cerebrovascular Diseases 33: 419-429, 2012
Persson PB, Bondke Persson A: Age your garlic for longevity. Acta Physiologica (Oxford) 205: 1-2, 2012
Bondke Persson A and Persson PB: Let 'em grow: the Yin and Yang of vessel growth. Acta Physiologica (Oxford) 204: 466-468, 2012
Bondke Persson A and Persson, PB: Getting a kick out of thermoregulation. Acta Physiologica (Oxford) 204: 291-293, 2012
Bondke Persson A, Buschmann E-E, Lindhorst R, Troidl K, Langhoff R, Schulte K-L, Buschmann I: Therapeutic arteriogenesis in peripheral arterial disease: combining intervention and passive training. Vasa 40:177-187, 2011
Scholz H, Kirschner KM: Oxygen-dependent gene expression in development and cancer: lessons learned from the Wilms' tumor gene, WT1. Front Mol Neurosci. 4, Article 4:1-11, 2011
Bondke Persson A, Buschmann IR: Vascular growth in health and disease. Frontiers in Molecular Neuroscience 4, 2011
Benko E, Winkelmann A, Meier JC, Persson PB, Scholz H, and Fähling M: Phorbol-ester mediated suppression of hASH1 synthesis: Multiple ways to keep the level down. Front Mol Neurosci. 4, Article 1:1-11, 2011
Sciesielski LK, Kirschner KM, Scholz H, Persson AB. Wilms' tumor protein Wt1 regulates the Interleukin-10 (IL-10) gene. FEBS Letters 584:4665-4671, 2010.
Kirschner KM, Sciesielski LK, Scholz H. Wilms' tumor protein Wt1 stimulates transcription of the gene encoding vascular endothelial cadherin. Pflügers Arch.-Europ. J. Physiol. 460:1051-1061, 2010.