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Article: Tuberoinfundibular Peptide of 39 residues is required for germ cell development.

Usdin, Ted B / Paciga, Mark / Riordan, Tim / Kuo, Jonathan / Parmelee, Alissa / Petukova, Galina / Camerini-Otero, R Daniel / Mezey, Eva

Endocrinology

2008 Volume 149, Issue 9, Page(s) 4292–4300

Abstract: Tuberoinfundibular peptide of 39 residues (TIP39) was identified as a PTH 2 receptor ligand. We report that mice with deletion of Tifp39, the gene encoding TIP39, are sterile. Testes contained Leydig and Sertoli cells and spermatogonia but no spermatids. ...

Abstract	Tuberoinfundibular peptide of 39 residues (TIP39) was identified as a PTH 2 receptor ligand. We report that mice with deletion of Tifp39, the gene encoding TIP39, are sterile. Testes contained Leydig and Sertoli cells and spermatogonia but no spermatids. Labeling chromosome spreads with antibodies to proteins involved in recombination showed that spermatogonia do not complete prophase of meiosis I. Chromosomes were observed at different stages of recombination in single nuclei, a defect not previously described with mutations in genes known to be specifically involved in DNA replication and recombination. TIP39 was previously shown to be expressed in neurons projecting to the hypothalamus and within the testes. LH and FSH were slightly elevated in Tifp39(-/-) mice, suggesting intact hypothalamic function. We found using in situ hybridization that the genes encoding TIP39 and the PTH 2 receptor are expressed in a stage-specific manner within seminiferous tubules. Using immunohistochemistry and quantitative RT-PCR, TIP39 expression is greatest in mature testes, and appears most abundant in postmeiotic spermatids, but TIP39 protein and mRNA can be detected before any cells have completed meiosis. We used mice that express Cre recombinase under control of a spermatid-specific promoter to express selectively a cDNA encoding TIP39 in the testes of Tifp39(-/-) mice. Spermatid production and fertility were rescued, demonstrating that the defect in Tifp39(-/-) mice was due to the loss of TIP39. These results show that TIP39 is essential for germ cell development and suggest that it may act as an autocrine or paracrine agent within the gonads.
MeSH term(s)	Animals ; Autocrine Communication/genetics ; Embryo, Mammalian ; Germ Cells/growth & development ; Germ Cells/metabolism ; Hormones/blood ; Male ; Meiosis/genetics ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Neuropeptides/genetics ; Neuropeptides/metabolism ; Neuropeptides/physiology ; Paracrine Communication/genetics ; RNA, Messenger/metabolism ; Spermatogenesis/genetics ; Testis/growth & development ; Testis/metabolism
Chemical Substances	Hormones ; Neuropeptides ; RNA, Messenger ; tuberoinfundibular peptide 39
Language	English
Publishing date	2008-05-15
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Intramural
ZDB-ID	427856-2
ISSN	1945-7170 ; 0013-7227
ISSN (online)	1945-7170
ISSN	0013-7227
DOI	10.1210/en.2008-0419
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Article: Ewing sarcoma gene EWS is essential for meiosis and B lymphocyte development.

Li, Hongjie / Watford, Wendy / Li, Cuiling / Parmelee, Alissa / Bryant, Mark A / Deng, Chuxia / O'Shea, John / Lee, Sean Bong

The Journal of clinical investigation

2007 Volume 117, Issue 5, Page(s) 1314–1323

Abstract: Ewing sarcoma gene EWS encodes a putative RNA-binding protein with proposed roles in transcription and splicing, but its physiological role in vivo remains undefined. Here, we have generated Ews-deficient mice and demonstrated that EWS is required for ... ...

Abstract	Ewing sarcoma gene EWS encodes a putative RNA-binding protein with proposed roles in transcription and splicing, but its physiological role in vivo remains undefined. Here, we have generated Ews-deficient mice and demonstrated that EWS is required for the completion of B cell development and meiosis. Analysis of Ews(-/-) lymphocytes revealed a cell-autonomous defect in precursor B lymphocyte (pre-B lymphocyte) development. During meiosis, Ews-null spermatocytes were deficient in XY bivalent formation and showed reduced meiotic recombination, resulting in massive apoptosis and complete arrest in gamete maturation. Inactivation of Ews in mouse embryonic fibroblasts resulted in premature cellular senescence, and the mutant animals showed hypersensitivity to ionizing radiation. Finally, we showed that EWS interacts with lamin A/C and that loss of EWS results in a reduced lamin A/C expression. Our findings reveal essential functions for EWS in pre-B cell development and meiosis, with proposed roles in DNA pairing and recombination/repair mechanisms. Furthermore, we demonstrate a novel role of EWS in cellular senescence, possibly through its interaction and modulation of lamin A/C.
MeSH term(s)	Animals ; Animals, Newborn ; B-Lymphocyte Subsets/cytology ; B-Lymphocyte Subsets/metabolism ; Cell Differentiation/genetics ; Cell Differentiation/physiology ; Cell Line, Tumor ; Embryonic Stem Cells/physiology ; Female ; HeLa Cells ; Humans ; Male ; Meiosis/genetics ; Meiosis/physiology ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; RNA-Binding Protein EWS/deficiency ; RNA-Binding Protein EWS/genetics ; RNA-Binding Protein EWS/physiology ; Retrospective Studies ; Sarcoma, Ewing/genetics ; Sarcoma, Ewing/metabolism ; Sarcoma, Ewing/pathology
Chemical Substances	RNA-Binding Protein EWS
Language	English
Publishing date	2007-04-05
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Intramural
ZDB-ID	3067-3
ISSN	1558-8238 ; 0021-9738
ISSN (online)	1558-8238
ISSN	0021-9738
DOI	10.1172/JCI31222
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Article ; Online: Characterization and function of histamine receptors in human bone marrow stromal cells.

Nemeth, Krisztian / Wilson, Todd / Rada, Balazs / Parmelee, Alissa / Mayer, Balazs / Buzas, Edit / Falus, Andras / Key, Sharon / Masszi, Tamas / Karpati, Sarolta / Mezey, Eva

Stem cells (Dayton, Ohio)

2011 Volume 30, Issue 2, Page(s) 222–231

Abstract: There are several clinical trials worldwide using bone marrow stromal cells (BMSCs) as a cellular therapy to modulate immune responses in patients suffering from various inflammatory conditions. A deeper understanding of the molecular mechanisms involved ...

Abstract	There are several clinical trials worldwide using bone marrow stromal cells (BMSCs) as a cellular therapy to modulate immune responses in patients suffering from various inflammatory conditions. A deeper understanding of the molecular mechanisms involved in this modulatory effect could help us design better, more effective protocols to treat immune mediated diseases. In this study, we demonstrated that human BMSCs express H1, H2, and H4 histamine receptors and they respond to histamine stimulation with an increased interleukin 6 (IL-6) production both in vitro and in vivo. Using different receptor antagonists, we pinpointed the importance of the H1 histamine receptor, while Western blot analysis and application of various mitogen-activated protein kinase inhibitors highlighted the role of p38, extracellular signal-regulated kinase, and c-Jun N-terminal kinase kinases in the observed effect. When BMSCs were pretreated with either histamine or degranulated human mast cells, they exhibited an enhanced IL-6-dependent antiapoptotic effect on neutrophil granulocytes. Based on these observations, it is likely that introduction of BMSCs into a histamine-rich environment (such as any allergic setting) or pretreatment of these cells with synthetic histamine could have a significant modulatory effect on the therapeutic potential of BMSCs.
MeSH term(s)	Animals ; Apoptosis ; Bone Marrow Cells/metabolism ; Bone Marrow Cells/physiology ; Cells, Cultured ; Coculture Techniques ; Gene Expression ; Granulocytes/metabolism ; Histamine/pharmacology ; Histamine/physiology ; Humans ; Interleukin-6/metabolism ; Interleukin-8/metabolism ; MAP Kinase Signaling System ; Male ; Mast Cells/metabolism ; Mice ; Mice, Inbred BALB C ; Mice, Inbred C57BL ; Receptors, Histamine/genetics ; Receptors, Histamine/metabolism ; Receptors, Histamine/physiology ; Stromal Cells/metabolism ; Stromal Cells/physiology
Chemical Substances	Interleukin-6 ; Interleukin-8 ; Receptors, Histamine ; Histamine (820484N8I3)
Language	English
Publishing date	2011-11-02
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	1143556-2
ISSN	1549-4918 ; 1066-5099
ISSN (online)	1549-4918
ISSN	1066-5099
DOI	10.1002/stem.771
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Article: DNA damage-induced BARD1 phosphorylation is critical for the inhibition of messenger RNA processing by BRCA1/BARD1 complex.

Kim, Ho-Shik / Li, Hongjie / Cevher, Murat / Parmelee, Alissa / Fonseca, Danae / Kleiman, Frida Esther / Lee, Sean Bong

Cancer research

2006 Volume 66, Issue 9, Page(s) 4561–4565

Abstract: BRCA1-associated RING domain protein BARD1, along with its heterodimeric partner BRCA1, plays important roles in cellular response to DNA damage. Immediate cellular response to genotoxic stress is mediated by a family of phosphoinositide 3-kinase-related ...

Abstract	BRCA1-associated RING domain protein BARD1, along with its heterodimeric partner BRCA1, plays important roles in cellular response to DNA damage. Immediate cellular response to genotoxic stress is mediated by a family of phosphoinositide 3-kinase-related protein kinases, such as ataxia-telangiectasia mutated (ATM), ATM and Rad3-related, and DNA-dependent protein kinase. ATM-mediated phosphorylation of BRCA1 enhances the DNA damage checkpoint functions of BRCA1, but how BARD1 is regulated during DNA damage signaling has not been examined. Here, we report that BARD1 undergoes phosphorylation upon ionizing radiation or UV radiation and identify Thr(714) as the in vivo BARD1 phosphorylation site. Importantly, DNA damage functions of BARD1 (i.e., inhibition of pre-mRNA polyadenylation and degradation of RNA polymerase II) are abrogated in T714A and T734A mutants. Our findings suggest that phosphorylation of BARD1 is critical for the DNA damage functions of the BRCA1/BARD1 complex.
MeSH term(s)	Amino Acid Sequence ; BRCA1 Protein/antagonists & inhibitors ; BRCA1 Protein/metabolism ; Bone Neoplasms/genetics ; Bone Neoplasms/metabolism ; Cell Line, Tumor ; Conserved Sequence ; DNA Damage/physiology ; Humans ; Molecular Sequence Data ; Osteosarcoma/genetics ; Osteosarcoma/metabolism ; Phosphatidylinositol 3-Kinases/metabolism ; Phosphorylation ; RNA, Messenger/antagonists & inhibitors ; RNA, Messenger/genetics ; RNA, Messenger/metabolism ; Transfection ; Tumor Suppressor Proteins/antagonists & inhibitors ; Tumor Suppressor Proteins/genetics ; Tumor Suppressor Proteins/metabolism ; Tumor Suppressor Proteins/radiation effects ; Ubiquitin-Protein Ligases/antagonists & inhibitors ; Ubiquitin-Protein Ligases/genetics ; Ubiquitin-Protein Ligases/metabolism ; Ubiquitin-Protein Ligases/radiation effects
Chemical Substances	BRCA1 Protein ; RNA, Messenger ; Tumor Suppressor Proteins ; BARD1 protein, human (EC 2.3.2.27) ; Ubiquitin-Protein Ligases (EC 2.3.2.27) ; Phosphatidylinositol 3-Kinases (EC 2.7.1.-)
Language	English
Publishing date	2006-05-01
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, N.I.H., Intramural
ZDB-ID	1432-1
ISSN	1538-7445 ; 0008-5472
ISSN (online)	1538-7445
ISSN	0008-5472
DOI	10.1158/0008-5472.CAN-05-3629
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Article ; Online: Bone marrow stromal cells attenuate sepsis via prostaglandin E(2)-dependent reprogramming of host macrophages to increase their interleukin-10 production.

Németh, Krisztián / Leelahavanichkul, Asada / Yuen, Peter S T / Mayer, Balázs / Parmelee, Alissa / Doi, Kent / Robey, Pamela G / Leelahavanichkul, Kantima / Koller, Beverly H / Brown, Jared M / Hu, Xuzhen / Jelinek, Ivett / Star, Robert A / Mezey, Eva

Nature medicine

2008 Volume 15, Issue 1, Page(s) 42–49

Abstract: Sepsis causes over 200,000 deaths yearly in the US; better treatments are urgently needed. Administering bone marrow stromal cells (BMSCs -- also known as mesenchymal stem cells) to mice before or shortly after inducing sepsis by cecal ligation and ... ...

Abstract	Sepsis causes over 200,000 deaths yearly in the US; better treatments are urgently needed. Administering bone marrow stromal cells (BMSCs -- also known as mesenchymal stem cells) to mice before or shortly after inducing sepsis by cecal ligation and puncture reduced mortality and improved organ function. The beneficial effect of BMSCs was eliminated by macrophage depletion or pretreatment with antibodies specific for interleukin-10 (IL-10) or IL-10 receptor. Monocytes and/or macrophages from septic lungs made more IL-10 when prepared from mice treated with BMSCs versus untreated mice. Lipopolysaccharide (LPS)-stimulated macrophages produced more IL-10 when cultured with BMSCs, but this effect was eliminated if the BMSCs lacked the genes encoding Toll-like receptor 4, myeloid differentiation primary response gene-88, tumor necrosis factor (TNF) receptor-1a or cyclooxygenase-2. Our results suggest that BMSCs (activated by LPS or TNF-alpha) reprogram macrophages by releasing prostaglandin E(2) that acts on the macrophages through the prostaglandin EP2 and EP4 receptors. Because BMSCs have been successfully given to humans and can easily be cultured and might be used without human leukocyte antigen matching, we suggest that cultured, banked human BMSCs may be effective in treating sepsis in high-risk patient groups.
MeSH term(s)	Animals ; Bone Marrow Cells/physiology ; Bone Marrow Transplantation/physiology ; Cecal Diseases/complications ; Cecal Diseases/mortality ; Cecal Diseases/physiopathology ; Cecal Diseases/therapy ; Cecum/injuries ; Cecum/pathology ; Cellular Reprogramming/immunology ; Cellular Reprogramming/physiology ; Dinoprostone/physiology ; Humans ; Interleukin-10/biosynthesis ; Interleukin-10/blood ; Macrophages/metabolism ; Male ; Mice ; Mice, Inbred BALB C ; Mice, Inbred C57BL ; Models, Biological ; Sepsis/etiology ; Sepsis/metabolism ; Sepsis/mortality ; Sepsis/therapy ; Stromal Cells/physiology ; Stromal Cells/transplantation ; Survival Analysis ; Transplantation ; Wounds, Penetrating/complications ; Wounds, Penetrating/mortality ; Wounds, Penetrating/physiopathology ; Wounds, Penetrating/therapy
Chemical Substances	Interleukin-10 (130068-27-8) ; Dinoprostone (K7Q1JQR04M)
Language	English
Publishing date	2008-11-21
Publishing country	United States
Document type	Evaluation Study ; Journal Article ; Research Support, N.I.H., Intramural
ZDB-ID	1220066-9
ISSN	1546-170X ; 1078-8956
ISSN (online)	1546-170X
ISSN	1078-8956
DOI	10.1038/nm.1905
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Zs.A 4212: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (2.OG) ab Jg. 2022: Lesesaal (EG)
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Article ; Online: The combination of granulocyte colony-stimulating factor and stem cell factor significantly increases the number of bone marrow-derived endothelial cells in brains of mice following cerebral ischemia.

Toth, Zsuzsanna E / Leker, Ronen R / Shahar, Tal / Pastorino, Sandra / Szalayova, Ildiko / Asemenew, Brook / Key, Sharon / Parmelee, Alissa / Mayer, Balazs / Nemeth, Krisztian / Bratincsák, Andras / Mezey, Eva

Blood

2008 Volume 111, Issue 12, Page(s) 5544–5552

Abstract: Granulocyte colony-stimulating factor (G-CSF) induces proliferation of bone marrow-derived cells. G-CSF is neuroprotective after experimental brain injury, but the mechanisms involved remain unclear. Stem cell factor (SCF) is a cytokine important for the ...

Abstract	Granulocyte colony-stimulating factor (G-CSF) induces proliferation of bone marrow-derived cells. G-CSF is neuroprotective after experimental brain injury, but the mechanisms involved remain unclear. Stem cell factor (SCF) is a cytokine important for the survival and differentiation of hematopoietic stem cells. Its receptor (c-kit or CD117) is present in some endothelial cells. We aimed to determine whether the combination of G-CSF/SCF induces angiogenesis in the central nervous system by promoting entry of endothelial precursors into the injured brain and causing them to proliferate there. We induced permanent middle cerebral artery occlusion in female mice that previously underwent sex-mismatched bone marrow transplantation from enhanced green fluorescent protein (EGFP)-expressing mice. G-CSF/SCF treatment reduced infarct volumes by more than 50% and resulted in a 1.5-fold increase in vessel formation in mice with stroke, a large percentage of which contain endothelial cells of bone marrow origin. Most cells entering the brain maintained their bone marrow identity and did not transdifferentiate into neural cells. G-CSF/SCF treatment also led to a 2-fold increase in the number of newborn cells in the ischemic hemisphere. These findings suggest that G-CSF/SCF treatment might help recovery through induction of bone marrow-derived angiogenesis, thus improving neuronal survival and functional outcome.
MeSH term(s)	Animals ; Bone Marrow Transplantation ; Brain Ischemia/drug therapy ; Brain Ischemia/pathology ; Cell Division/drug effects ; Drug Therapy, Combination ; Endothelial Cells/cytology ; Endothelial Cells/drug effects ; Female ; Granulocyte Colony-Stimulating Factor/pharmacology ; Green Fluorescent Proteins ; Infarction, Middle Cerebral Artery/drug therapy ; Infarction, Middle Cerebral Artery/pathology ; Mice ; Mice, Inbred C57BL ; Neovascularization, Physiologic/drug effects ; Recovery of Function/drug effects ; Stem Cell Factor/pharmacology
Chemical Substances	Stem Cell Factor ; Granulocyte Colony-Stimulating Factor (143011-72-7) ; Green Fluorescent Proteins (147336-22-9)
Language	English
Publishing date	2008-02-11
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Intramural ; Research Support, Non-U.S. Gov't
ZDB-ID	80069-7
ISSN	1528-0020 ; 0006-4971
ISSN (online)	1528-0020
ISSN	0006-4971
DOI	10.1182/blood-2007-10-119073
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Article: Tuberoinfundibular Peptide of 39 residues is required for germ cell development.

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Article: Ewing sarcoma gene EWS is essential for meiosis and B lymphocyte development.

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Article ; Online: Characterization and function of histamine receptors in human bone marrow stromal cells.

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Article: DNA damage-induced BARD1 phosphorylation is critical for the inhibition of messenger RNA processing by BRCA1/BARD1 complex.

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Article ; Online: Bone marrow stromal cells attenuate sepsis via prostaglandin E(2)-dependent reprogramming of host macrophages to increase their interleukin-10 production.

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Article ; Online: The combination of granulocyte colony-stimulating factor and stem cell factor significantly increases the number of bone marrow-derived endothelial cells in brains of mice following cerebral ischemia.

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