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Article ; Online: Dipeptidase-1 governs renal inflammation during ischemia reperfusion injury.

Lau, Arthur / Rahn, Jennifer J / Chappellaz, Mona / Chung, Hyunjae / Benediktsson, Hallgrimur / Bihan, Dominique / von Mässenhausen, Anne / Linkermann, Andreas / Jenne, Craig N / Robbins, Stephen M / Senger, Donna L / Lewis, Ian A / Chun, Justin / Muruve, Daniel A

Science advances

2022 Volume 8, Issue 5, Page(s) eabm0142

Abstract: The mechanisms that drive leukocyte recruitment to the kidney are incompletely understood. Dipeptidase-1 (DPEP1) is a major neutrophil adhesion receptor highly expressed on proximal tubular cells and peritubular capillaries of the kidney. Renal ischemia ... ...

Abstract	The mechanisms that drive leukocyte recruitment to the kidney are incompletely understood. Dipeptidase-1 (DPEP1) is a major neutrophil adhesion receptor highly expressed on proximal tubular cells and peritubular capillaries of the kidney. Renal ischemia reperfusion injury (IRI) induces robust neutrophil and monocyte recruitment and causes acute kidney injury (AKI). Renal inflammation and the AKI phenotype were attenuated in
MeSH term(s)	Acute Kidney Injury/etiology ; Animals ; Dipeptidases/metabolism ; Female ; GPI-Linked Proteins/metabolism ; Humans ; Inflammation/complications ; Male ; Mice ; Mice, Inbred C57BL ; Reperfusion Injury
Chemical Substances	GPI-Linked Proteins ; Dipeptidases (EC 3.4.13.-) ; dipeptidase (EC 3.4.13.18) ; dipeptidase 1 (EC 3.4.13.19)
Language	English
Publishing date	2022-02-02
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2810933-8
ISSN	2375-2548 ; 2375-2548
ISSN (online)	2375-2548
ISSN	2375-2548
DOI	10.1126/sciadv.abm0142
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Article ; Online: Opa1 is required for proper mitochondrial metabolism in early development.

Rahn, Jennifer J / Stackley, Krista D / Chan, Sherine S L

PloS one

2013 Volume 8, Issue 3, Page(s) e59218

Abstract: Opa1 catalyzes fusion of inner mitochondrial membranes and formation of the cristae. OPA1 mutations in humans lead to autosomal dominant optic atrophy. OPA1 knockout mice lose viability around embryonic day 9 from unknown reasons, indicating that OPA1 is ...

Abstract	Opa1 catalyzes fusion of inner mitochondrial membranes and formation of the cristae. OPA1 mutations in humans lead to autosomal dominant optic atrophy. OPA1 knockout mice lose viability around embryonic day 9 from unknown reasons, indicating that OPA1 is essential for embryonic development. Zebrafish are an attractive model for studying vertebrate development and have been used for many years to describe developmental events that are difficult or impractical to view in mammalian models. In this study, Opa1 was successfully depleted in zebrafish embryos using antisense morpholinos, which resulted in disrupted mitochondrial morphology. Phenotypically, these embryos exhibited abnormal blood circulation and heart defects, as well as small eyes and small pectoral fin buds. Additionally, startle response was reduced and locomotor activity was impaired. Furthermore, Opa1 depletion caused bioenergetic defects, without impairing mitochondrial efficiency. In response to mitochondrial dysfunction, a transient upregulation of the master regulator of mitochondrial biogenesis, pgc1a, was observed. These results not only reveal a new Opa1-associated phenotype in a vertebrate model system, but also further elucidates the absolute requirement of Opa1 for successful vertebrate development.
MeSH term(s)	Animals ; Blotting, Western ; Mitochondria/drug effects ; Mitochondria/genetics ; Mitochondria/metabolism ; Morpholinos/pharmacology ; Zebrafish/embryology ; Zebrafish/genetics ; Zebrafish/metabolism ; Zebrafish Proteins/antagonists & inhibitors ; Zebrafish Proteins/genetics ; Zebrafish Proteins/metabolism
Chemical Substances	Morpholinos ; Zebrafish Proteins
Language	English
Publishing date	2013-03-14
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ISSN	1932-6203
ISSN (online)	1932-6203
DOI	10.1371/journal.pone.0059218
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Article ; Online: Use of gene targeting to study recombination in mammalian cell DNA repair mutants.

Rahn, Jennifer J / Adair, Gerald M / Nairn, Rodney S

Methods in molecular biology (Clifton, N.J.)

2012 Volume 920, Page(s) 445–470

Abstract: The study of gene function has been greatly facilitated by the development of strategies to modify genomic DNA. Gene targeting is one of the most successfully applied techniques used to examine the roles of specific genes in a wide variety of model ... ...

Abstract	The study of gene function has been greatly facilitated by the development of strategies to modify genomic DNA. Gene targeting is one of the most successfully applied techniques used to examine the roles of specific genes in a wide variety of model systems from yeast to mammals. Our laboratory has pioneered the use of the Chinese hamster ovary (CHO) cell culture model system to study pathways of DNA repair and recombination at the hemizygous CHO APRT locus. By using a simple and effective gene targeting method, we have generated a number of DNA repair-deficient cell lines that have been used in targeted recombination experiments to investigate pathways of recombinational repair in somatic mammalian cells. These methods can be readily customized to generate a variety of cell lines deficient in specific genes of interest and can be applied to study the roles of other DNA repair proteins in pathways of mammalian recombinational repair.
MeSH term(s)	Adenine Phosphoribosyltransferase/deficiency ; Adenine Phosphoribosyltransferase/genetics ; Animals ; CHO Cells ; Cell Culture Techniques ; Clone Cells ; Cricetinae ; Cricetulus ; DNA Repair ; Electroporation ; Gene Knockout Techniques ; Gene Targeting/methods ; Genetic Loci/genetics ; Genetic Vectors/genetics ; Mutation ; Recombination, Genetic
Chemical Substances	Adenine Phosphoribosyltransferase (EC 2.4.2.7)
Language	English
Publishing date	2012
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ISSN	1940-6029
ISSN (online)	1940-6029
DOI	10.1007/978-1-61779-998-3_31
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Article ; Online: Development of a peptide-based delivery platform for targeting malignant brain tumors.

Rahn, Jennifer J / Lun, Xueqing / Jorch, Selina K / Hao, Xiaoguang / Venugopal, Chitra / Vora, Parvez / Ahn, Bo Young / Babes, Liane / Alshehri, Mana M / Cairncross, J Gregory / Singh, Sheila K / Kubes, Paul / Senger, Donna L / Robbins, Stephen M

Biomaterials

2020 Volume 252, Page(s) 120105

Abstract: Despite extensive molecular characterization, human glioblastoma remains a fatal disease with survival rates measured in months. Little improvement is seen with standard surgery, radiotherapy and chemotherapy. Clinical progress is hampered by the ... ...

Abstract	Despite extensive molecular characterization, human glioblastoma remains a fatal disease with survival rates measured in months. Little improvement is seen with standard surgery, radiotherapy and chemotherapy. Clinical progress is hampered by the inability to detect and target glioblastoma disease reservoirs based on a diffuse invasive pattern and the presence of molecular and phenotypic heterogeneity. The goal of this study was to target the invasive and stem-like glioblastoma cells that evade first-line treatments using agents capable of delivering imaging enhancers or biotherapeutic cargo. To accomplish this, a combinatorial phage display library was biopanned against glioblastoma cell model systems that accurately recapitulate the intra- and inter-tumor heterogeneity and infiltrative nature of the disease. Candidate peptides were screened for specificity and ability to target glioblastoma cells in vivo. Cargo-conjugated peptides delivered contrast-enhancing agents to highly infiltrative tumor populations in intracranial xenograft models without the obvious need for blood brain barrier disruption. Simultaneous use of five independent targeting peptides provided greater coverage of this complex tumor and selected peptides have the capacity to deliver a therapeutic cargo (oncolytic virus VSVΔM51) to the tumor cells in vivo. Herein, we have identified a series of peptides with utility as an innovative platform to assist in targeting glioblastoma for the purpose of diagnostic or prognostic imaging, image-guided surgery, and/or improved delivery of therapeutic agents to glioblastoma cells implicated in disease relapse.
MeSH term(s)	Animals ; Brain Neoplasms ; Cell Line, Tumor ; Glioblastoma/drug therapy ; Humans ; Oncolytic Viruses ; Peptides
Chemical Substances	Peptides
Language	English
Publishing date	2020-05-07
Publishing country	Netherlands
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	603079-8
ISSN	1878-5905 ; 0142-9612
ISSN (online)	1878-5905
ISSN	0142-9612
DOI	10.1016/j.biomaterials.2020.120105
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Article: Development of a peptide-based delivery platform for targeting malignant brain tumors

Rahn, Jennifer J / Lun, Xueqing / Jorch, Selina K / Hao, Xiaoguang / Venugopal, Chitra / Vora, Parvez / Ahn, Bo Young / Babes, Liane / Alshehri, Mana M / Cairncross, J. Gregory / Singh, Sheila K / Kubes, Paul / Senger, Donna L / Robbins, Stephen M

Biomaterials. 2020 Sept., v. 252

2020

Abstract	Despite extensive molecular characterization, human glioblastoma remains a fatal disease with survival rates measured in months. Little improvement is seen with standard surgery, radiotherapy and chemotherapy. Clinical progress is hampered by the inability to detect and target glioblastoma disease reservoirs based on a diffuse invasive pattern and the presence of molecular and phenotypic heterogeneity. The goal of this study was to target the invasive and stem-like glioblastoma cells that evade first-line treatments using agents capable of delivering imaging enhancers or biotherapeutic cargo. To accomplish this, a combinatorial phage display library was biopanned against glioblastoma cell model systems that accurately recapitulate the intra- and inter-tumor heterogeneity and infiltrative nature of the disease. Candidate peptides were screened for specificity and ability to target glioblastoma cells in vivo. Cargo-conjugated peptides delivered contrast-enhancing agents to highly infiltrative tumor populations in intracranial xenograft models without the obvious need for blood brain barrier disruption. Simultaneous use of five independent targeting peptides provided greater coverage of this complex tumor and selected peptides have the capacity to deliver a therapeutic cargo (oncolytic virus VSVΔM51) to the tumor cells in vivo. Herein, we have identified a series of peptides with utility as an innovative platform to assist in targeting glioblastoma for the purpose of diagnostic or prognostic imaging, image-guided surgery, and/or improved delivery of therapeutic agents to glioblastoma cells implicated in disease relapse.
Keywords	bacteriophages ; biocompatible materials ; blood-brain barrier ; brain ; drug therapy ; glioblastoma ; humans ; peptides ; phenotypic variation ; radiotherapy ; relapse ; xenotransplantation
Language	English
Dates of publication	2020-09
Publishing place	Elsevier Ltd
Document type	Article
Note	NAL-AP-2-clean
ZDB-ID	603079-8
ISSN	0142-9612
ISSN	0142-9612
DOI	10.1016/j.biomaterials.2020.120105
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Article ; Online: Zebrafish lacking functional DNA polymerase gamma survive to juvenile stage, despite rapid and sustained mitochondrial DNA depletion, altered energetics and growth.

Rahn, Jennifer J / Bestman, Jennifer E / Stackley, Krista D / Chan, Sherine S L

Nucleic acids research

2015 Volume 43, Issue 21, Page(s) 10338–10352

Abstract: DNA polymerase gamma (POLG) is essential for replication and repair of mitochondrial DNA (mtDNA). Mutations in POLG cause mtDNA instability and a diverse range of poorly understood human diseases. Here, we created a unique Polg animal model, by modifying ...

Abstract	DNA polymerase gamma (POLG) is essential for replication and repair of mitochondrial DNA (mtDNA). Mutations in POLG cause mtDNA instability and a diverse range of poorly understood human diseases. Here, we created a unique Polg animal model, by modifying polg within the critical and highly conserved polymerase domain in zebrafish. polg(+/-) offspring were indistinguishable from WT siblings in multiple phenotypic and biochemical measures. However, polg(-/-) mutants developed severe mtDNA depletion by one week post-fertilization (wpf), developed slowly and had regenerative defects, yet surprisingly survived up to 4 wpf. An in vivo mtDNA polymerase activity assay utilizing ethidium bromide (EtBr) to deplete mtDNA, showed that polg(+/-) and WT zebrafish fully recover mtDNA content two weeks post-EtBr removal. EtBr further reduced already low levels of mtDNA in polg(-/-) animals, but mtDNA content did not recover following release from EtBr. Despite significantly decreased respiration that corresponded with tissue-specific levels of mtDNA, polg(-/-) animals had WT levels of ATP and no increase in lactate. This zebrafish model of mitochondrial disease now provides unique opportunities for studying mtDNA instability from multiple angles, as polg(-/-) mutants can survive to juvenile stage, rather than lose viability in embryogenesis as seen in Polg mutant mice.
MeSH term(s)	Adenosine Triphosphate/metabolism ; Animal Fins/physiology ; Animals ; DNA Polymerase gamma ; DNA, Mitochondrial/analysis ; DNA-Directed DNA Polymerase/chemistry ; DNA-Directed DNA Polymerase/genetics ; DNA-Directed DNA Polymerase/metabolism ; Genetic Engineering ; Glycolysis ; Models, Animal ; Mutation ; Oxygen Consumption ; Regeneration ; Survival Analysis ; Zebrafish/genetics ; Zebrafish/growth & development ; Zebrafish Proteins/chemistry ; Zebrafish Proteins/genetics ; Zebrafish Proteins/metabolism
Chemical Substances	DNA, Mitochondrial ; Zebrafish Proteins ; Adenosine Triphosphate (8L70Q75FXE) ; DNA Polymerase gamma (EC 2.7.7.7) ; DNA-Directed DNA Polymerase (EC 2.7.7.7)
Language	English
Publishing date	2015-12-02
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	186809-3
ISSN	1362-4962 ; 1362-4954 ; 0301-5610 ; 0305-1048
ISSN (online)	1362-4962 ; 1362-4954
ISSN	0301-5610 ; 0305-1048
DOI	10.1093/nar/gkv1139
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Article ; Online: The cellular and molecular progression of mitochondrial dysfunction induced by 2,4-dinitrophenol in developing zebrafish embryos.

Bestman, Jennifer E / Stackley, Krista D / Rahn, Jennifer J / Williamson, Tucker J / Chan, Sherine S L

Differentiation; research in biological diversity

2015 Volume 89, Issue 3-4, Page(s) 51–69

Abstract: The etiology of mitochondrial disease is poorly understood. Furthermore, treatment options are limited, and diagnostic methods often lack the sensitivity to detect disease in its early stages. Disrupted oxidative phosphorylation (OXPHOS) that inhibits ... ...

Abstract	The etiology of mitochondrial disease is poorly understood. Furthermore, treatment options are limited, and diagnostic methods often lack the sensitivity to detect disease in its early stages. Disrupted oxidative phosphorylation (OXPHOS) that inhibits ATP production is a common phenotype of mitochondrial disorders that can be induced in zebrafish by exposure to 2,4-dinitrophenol (DNP), a FDA-banned weight-loss agent and EPA-regulated environmental toxicant, traditionally used in research labs as an uncoupler of OXPHOS. Despite the DNP-induced OXPHOS inhibition we observed using in vivo respirometry, the development of the DNP-treated and control zebrafish were largely similar during the first half of embryogenesis. During this period, DNP-treated embryos induced gene expression of mitochondrial and nuclear genes that stimulated the production of new mitochondria and increased glycolysis to yield normal levels of ATP. DNP-treated embryos were incapable of sustaining this mitochondrial biogenic response past mid-embryogenesis, as shown by significantly lowered ATP production and ATP levels, decreased gene expression, and the onset of developmental defects. Examining neural tissues commonly affected by mitochondrial disease, we found that DNP exposure also inhibited motor neuron axon arbor outgrowth and the proper formation of the retina. We observed and quantified the molecular and physiological progression of mitochondrial dysfunction during development with this new model of OXPHOS dysfunction, which has great potential for use in diagnostics and therapies for mitochondrial disease.
MeSH term(s)	2,4-Dinitrophenol/toxicity ; Adenosine Triphosphate/biosynthesis ; Animals ; Embryonic Development/genetics ; Energy Metabolism/genetics ; Gene Expression Regulation, Developmental/drug effects ; Humans ; Mitochondria/genetics ; Mitochondria/metabolism ; Mitochondria/pathology ; Mitochondrial Diseases/chemically induced ; Mitochondrial Diseases/genetics ; Mitochondrial Diseases/metabolism ; Mitochondrial Diseases/pathology ; Motor Neurons/metabolism ; Motor Neurons/pathology ; Oxidative Phosphorylation/drug effects ; Retina/metabolism ; Retina/pathology ; Zebrafish
Chemical Substances	Adenosine Triphosphate (8L70Q75FXE) ; 2,4-Dinitrophenol (Q13SKS21MN)
Language	English
Publishing date	2015-03
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	184540-8
ISSN	1432-0436 ; 0301-4681
ISSN (online)	1432-0436
ISSN	0301-4681
DOI	10.1016/j.diff.2015.01.001
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Article ; Online: Multiple roles of ERCC1-XPF in mammalian interstrand crosslink repair.

Rahn, Jennifer J / Adair, Gerald M / Nairn, Rodney S

Environmental and molecular mutagenesis

2010 Volume 51, Issue 6, Page(s) 567–581

Abstract: DNA interstrand crosslinks (ICLs) are among the most deleterious cytotoxic lesions encountered by cells, mainly due to the covalent linkage these lesions create between the two strands of DNA which effectively blocks replication and transcription. ... ...

Abstract	DNA interstrand crosslinks (ICLs) are among the most deleterious cytotoxic lesions encountered by cells, mainly due to the covalent linkage these lesions create between the two strands of DNA which effectively blocks replication and transcription. Although ICL repair in mammalian cells is not fully understood, processing of these lesions is thought to begin by "unhooking" at the site of the damaged base accompanied by the generation of a double strand break and ultimately repair through translesion synthesis and homologous recombination. A key player in this repair process is the heterodimeric protein complex ERCC1-XPF. Although some models of ICL repair restrict ERCC1-XPF activity to the unhooking step, recent data suggest that this protein complex acts in additional downstream steps. Here, we review the evidence implicating ERCC1-XPF in multiple steps of ICL repair.
MeSH term(s)	Animals ; DNA Repair ; DNA-Binding Proteins/metabolism ; DNA-Binding Proteins/physiology ; Endonucleases/metabolism ; Humans ; Models, Biological
Chemical Substances	DNA-Binding Proteins ; xeroderma pigmentosum group F protein ; ERCC1 protein, human (EC 3.1.-) ; Endonucleases (EC 3.1.-)
Language	English
Publishing date	2010-07
Publishing country	United States
Document type	Journal Article ; Research Support, U.S. Gov't, P.H.S. ; Review
ZDB-ID	639145-x
ISSN	1098-2280 ; 0893-6692
ISSN (online)	1098-2280
ISSN	0893-6692
DOI	10.1002/em.20583
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Article ; Online: Elesclomol restores mitochondrial function in genetic models of copper deficiency.

Soma, Shivatheja / Latimer, Andrew J / Chun, Haarin / Vicary, Alison C / Timbalia, Shrishiv A / Boulet, Aren / Rahn, Jennifer J / Chan, Sherine S L / Leary, Scot C / Kim, Byung-Eun / Gitlin, Jonathan D / Gohil, Vishal M

Proceedings of the National Academy of Sciences of the United States of America

2018 Volume 115, Issue 32, Page(s) 8161–8166

Abstract: Copper is an essential cofactor of ... ...

Abstract	Copper is an essential cofactor of cytochrome
MeSH term(s)	Animals ; Antineoplastic Agents/pharmacology ; Antineoplastic Agents/therapeutic use ; Biological Transport/genetics ; Carrier Proteins/genetics ; Cell Line ; Coenzymes/deficiency ; Copper/deficiency ; Copper/therapeutic use ; Dietary Supplements ; Disease Models, Animal ; Drug Repositioning ; Drugs, Investigational/pharmacology ; Drugs, Investigational/therapeutic use ; Electron Transport Complex IV/metabolism ; Fibroblasts ; Humans ; Hydrazines/pharmacology ; Hydrazines/therapeutic use ; Membrane Transport Proteins/genetics ; Metabolism, Inborn Errors/drug therapy ; Metabolism, Inborn Errors/genetics ; Metabolism, Inborn Errors/metabolism ; Mitochondria/drug effects ; Mitochondria/metabolism ; Mitochondrial Proteins/genetics ; Mutagenesis, Site-Directed ; Mutation ; Rats ; Saccharomyces cerevisiae ; Zebrafish ; Zebrafish Proteins/genetics
Chemical Substances	Antineoplastic Agents ; COA6 protein, human ; Carrier Proteins ; Coenzymes ; Ctr1 protein, zebrafish ; Drugs, Investigational ; Hydrazines ; Membrane Transport Proteins ; Mitochondrial Proteins ; SCO2 protein, human ; Zebrafish Proteins ; elesclomol (6UK191M53P) ; Copper (789U1901C5) ; Electron Transport Complex IV (EC 1.9.3.1)
Language	English
Publishing date	2018-07-23
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	209104-5
ISSN	1091-6490 ; 0027-8424
ISSN (online)	1091-6490
ISSN	0027-8424
DOI	10.1073/pnas.1806296115
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Article ; Online: Bioenergetic profiling of zebrafish embryonic development.

Stackley, Krista D / Beeson, Craig C / Rahn, Jennifer J / Chan, Sherine S L

PloS one

2011 Volume 6, Issue 9, Page(s) e25652

Abstract: Many debilitating conditions are linked to bioenergetic defects. Developing screens to probe the genetic and/or chemical basis for such links has proved intractable. Furthermore, there is a need for a physiologically relevant assay of bioenergetics in ... ...

Abstract	Many debilitating conditions are linked to bioenergetic defects. Developing screens to probe the genetic and/or chemical basis for such links has proved intractable. Furthermore, there is a need for a physiologically relevant assay of bioenergetics in whole organisms, especially for early stages in life where perturbations could increase disease susceptibility with aging. Thus, we asked whether we could screen bioenergetics and mitochondrial function in the developing zebrafish embryo. We present a multiplexed method to assay bioenergetics in zebrafish embryos from the blastula period (3 hours post-fertilization, hpf) through to hatching (48 hpf). In proof of principle experiments, we measured respiration and acid extrusion of developing zebrafish embryos. We quantified respiratory coupling to various bioenergetic functions by using specific pharmacological inhibitors of bioenergetic pathways. We demonstrate that changes in the coupling to ATP turnover and proton leak are correlated with developmental stage. The multiwell format of this assay enables the user to screen for the effects of drugs and environmental agents on bioenergetics in the zebrafish embryo with high sensitivity and reproducibility.
MeSH term(s)	Adenosine Triphosphate/metabolism ; Animals ; Cell Respiration/drug effects ; Embryo, Nonmammalian/cytology ; Embryo, Nonmammalian/drug effects ; Embryo, Nonmammalian/metabolism ; Energy Metabolism/drug effects ; Extracellular Space/drug effects ; Extracellular Space/metabolism ; Hydrogen-Ion Concentration ; Linear Models ; Microarray Analysis/methods ; Mitochondria/drug effects ; Mitochondria/metabolism ; Protons ; Reproducibility of Results ; Zebrafish/embryology ; Zebrafish/metabolism
Chemical Substances	Protons ; Adenosine Triphosphate (8L70Q75FXE)
Language	English
Publishing date	2011-09-29
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2267670-3
ISSN	1932-6203 ; 1932-6203
ISSN (online)	1932-6203
ISSN	1932-6203
DOI	10.1371/journal.pone.0025652
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