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Science China(Life Sciences) 2019年第10期62卷 1375-1380页

作者： Elizabeth A. Hines Mary-Kayt N. Jones Julie F. Harvey Chad Perlyn David M. Ornitz Xin Sun Jamie M. Verheyden Laboratory of Genetics University of WisconsinMadisonWI 53706USA Department of Surgery Florida International University College of MedicineMiamiFL 33199USA Department of developmental Biology Washington University School of MedicineSt. LouisMO 63110USA Department of Pediatrics University of California-San DiegoLa JollaCA 92093USA

Crouzon syndrome is the result of a gain-of-function point mutation in FGFR2. Mimicking the human mutation, a mouse model of Crouzon syndrome(Fgfr2342Y) recapitulates patient deformities, including failed tracheal cartilage segmentation, resulting in a cartilaginous sleeve in the homozygous mutants. We found that the Fgfr2C342Y/C^342Y mutants exhibited an increase in chondrocytes prior to segmentation. This increase is due at least in part to over proliferation. Genetic ablation of chondrocytes in the mutant led to restoration of segmentation in the lateral but not central portion of the trachea. These results suggest that in the Fgfr2C342Y/C342Y mutants, increased cartilage cell proliferation precedes and contributes to the disruption of cartilage segmentation in the developing trachea.

关键词： trachea lung mouse development

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Pulsatile gonadotropin-releasing hormone therapy is associated with earlier spermatogenesis compared to combined gonadotropin therapy in patients with congenital hypogonadotropic hypogonadism

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Asian Journal of Andrology 2017年第6期19卷 680-685页

作者： Jiang-Feng Mao Zhao-Xiang Liu Min Nie Xi Wang Hong-Li Xu Bing-Kun Huang Jun-Jie Zheng Le Min Ursula Brigitte Kaiser Xue-Yan Wu Department of Endocrinology Peking Union Medical College Hospital Key Laboratory of Endocrinology Ministry of Health Beijing 100730 China Internal Department Division of Endocrinology Diabetes and Hypertension Brigham and Women's Hospital Harvard Medical School Boston MA 02115 USA.

Both pulsatile gonadotropin-releasing hormone （GnRH） infusion and combined gonadotropin therapy （human chorionic gonadotropin and human menopausal gonadotropin [HCG/HMG]） are effective to induce spermatogenesis in male patients with congenital hypogonadotropic hypogonadism （CH H）. However, evidence is lacking as to which treatment strategy is better. This retrospective cohort study included 202 patients with CHH： twenty had received pulsatile GnRH and 182 had received HCG/HMG. Patients had received therapy for at least 12 months. The total follow-up time was 15.6 ± 5.0 months （range： 12-27 months） for the GnRH group and 28.7 ± 13.0 months （range： 12-66 months） for the HCG/HMG group. The median time to first sperm appearance was 6 months （95% confidence interval [CI]： 1.6-10.4） in the GnRH group versus 18 months （95% Ch 16.4-20.0） in the HCG/HMG group （P〈 0.001）. The median time to achieve sperm concentrations 〉5 x 106 m1-1 was 14 months （95% Ch 5.8-22.2） in the GnRH group versus 27 months （95% Ch 18.9-35.1） in the HCG/HMG group （P 〈 0.001）, and the median time to concentrations 〉10 x 106 m1-1 was 18 months （95% Ch 10.0-26.0） in the GnRH group versus 39 months （95% CI unknown） in the HCG/HMG group. Compared to the GnRH group, the HCG/HMG group required longer treatment periods to achieve testicular sizes of 〉4 ml, 〉8 ml, 〉12 ml, and 〉16 ml. Sperm motility （a ＋ b ＋ c percentage） evaluated in semen samples with concentrations 〉1 × 106 ml-1 was 43.7% ± 20.4% （16 samples） in the GnRH group versus 43.2% ± 18.1% （153 samples） in the HCG/HMG group （P= 0.921）. Notably, during follow-up, the GnRH group had lower serum testosterone levels than the HCG/HMG group （8.3 ±4.6 vs 16.2 ± 8.2 nmol 1-1, P 〈 0.001）. Our study found that pulsatile GnRH therapy was associated with earlier spermatogenesis and larger testicular size compared to combined gonadotropin therapy. Additional prospective randomized studies would be required to confirm these findings.

关键词： combined gonadotropin therapy congenital hypogonadotropic hypogonadism pulsatile GnRH therapy spermatogenesis

Involvement of chromatin and histone acetylation in the regulation of HIV-LTR by thyroid hormone receptor

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Cell Research 2001年第1期11卷 8-16页

作者： SHAO CHUNG VICTOR HSIA, HUA WANG, YUN BO SHI (Unit on Molecular Morphogenesis, Laboratory of Molecular Embryology, national institute of child health and human development, national institute of health, Building 18T, Room 106, Bethesda, MD 20892-5431, USA Unit on Molecular Morphogenesis Laboratory of Molecular Embryology National Institute of Child Health and Human Development National Institute of Health Bethesda USA

The HIV-1 LTR controls the expression of HIV-1 viral genes and thus is critical for viral propagation and pathology. Numerous host factors have been shown to participate in the regulation of the LTR Promoter. Among them is the thyroid hormone (T3) receptor (TR). TR has been shown to bind to the critical region of the promoter that contain the NFkB and Sp1 binding sites. Interestingly, earlier transient transfection studies in tissue culture cells have yielded contradicting conclusions on the role of TR in LTR regulation, likely due to the use of different cell types and/or lack of proper chromatin organization. Here, using the frog oocyte as a model system that allows replication-coupled chromatin assembly, mimicking that in somatic cells, we demonstrate that unliganded heterodimers of TR and RXR (9-cis retinoic acid receptor) repress LTR while the addition of T3 relieves the repression and further activates the promoter. More importantly, we show that chromatin and unliganded TR/RXR synergize to repress the promoter in a histone deacetylase- dependent manner.

关键词： HIV thyroid hormone receptor histone acetylation transcriptional repression Xenopus oocyte.

Immune cells in term and preterm labor

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Cellular & Molecular Immunology 2014年第6期11卷 571-581页

作者： Nardhy Gomez-Lopez Derek StLouis Marcus A Lehr Elly N Sanchez-Rodriguez Marcia Arenas-Hernandez Department of Obstetrics & Gynecology and Immunology & Microbiology Wayne State University Detroit MI USA Perinatology Research Branch nichd/NIH School of Medicine Wayne State University Detroit MI USA

Labor resembles an inflammatory response that includes secretion of cytokines/chemokines by resident and infiltrating immune cells into reproductive tissues and the maternal/fetal interface. Untimely activation of these inflammatory pathways leads to preterm labor, which can result in preterm birth. Preterm birth is a major determinant of neonatal mortality and morbidity; therefore, the elucidation of the process of labor at a cellular and molecular level is essential for understanding the pathophysiology of preterm labor. Here, we summarize the role of innate and adaptive immune cells in the physiological or pathological activation of labor. We review published literature regarding the role of innate and adaptive immune cells in the cervix, myometrium, fetal membranes, decidua and the fetus in late pregnancy and labor at term and preterm. Accumulating evidence suggests that innate immune cells （neutrophils, macrophages and mast cells） mediate the process of labor by releasing pro-inflammatory factors such as cytokines, chemokines and matrix metalloproteinases. Adaptive immune cells （T-cell subsets and B cells） participate in the maintenance of fetomaternal tolerance during pregnancy, and an alteration in their function or abundance may lead to labor at term or preterm. Also, immune cells that bridge the innate and adaptive immune systems （natural killer T （NKT） cells and dendritic cells （DCs）） seem to participate in the pathophysiology of preterm labor. In conclusion, a balance between innate and adaptive immune cells is required in order to sustain pregnancy; an alteration of this balance will lead to labor at term or preterm.

关键词： B cells cytotoxic T cells dendritic cells macrophages mast cells neutrophils NKT cells parturition preterm delivery regulatory T cells T cells

The matrix metalloproteinase stromelysin-3 cleaves laminin receptor at two distinct sites between the transmembrane domain and laminin binding sequence within the extracellular domain

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Cell Research 2005年第3期15卷 150-159页

作者： Tosikazu AMANO,Olivia KWAK,Anastasia MARSHAK Laboratory of Gene Regulation and development national institute of child health and human development national institutesof health Bethesda MD 20892 USA Laboratory of Gene Regulation and development national institute of child health and human development national institutesof health Bethesda MD 20892 USA Laboratory of Gene Regulation and development national institute of child health and human development national institutesof health Bethesda MD 20892 USA

The matrix metalloproteinase (MMP) stromelysin-3 (ST3) has long been implicated to play an important role in extracellular matrix (ECM) remodeling and cell fate determination during normal and pathological processes. However like other MMPs, the molecular basis of ST3 function in vivo remains unclear due to the lack of information on its physiological substrates. Furthermore, ST3 has only weak activities toward all tested ECM proteins. Using thyroid hormone-dependent Xenopus laevis metamorphosis as a model, we demonstrated previously that ST3 is important for apoptosis and tissue morphogenesis during intestinal remodeling. Here, we used yeast two-hybrid screen with mRNAs from metamorphosing tadpoles to identify potential substrate of ST3 during development. We thus isolated the 37 kd laminin receptor precursor (LR). We showed that LR binds to ST3 in vitro and can be cleaved by ST3 at two sites distinct from where other MMPs cleave. Through peptide sequencing, we determined that the two cleavage sites are in the extracellular domain between the transmembrane domain and laminin binding sequence. Furthermore, we demon strated that these cleavage sites are conserved in human LR. These results together with high levels of human LR and ST3 expression in carcinomas suggest that LR is a likely in vivo substrate of ST3 and that its cleavage by ST3 may alter cell-extracellular matrix interaction, thus, playing a role in mediating the effects of ST3 on cell fate and behavior ob- served during development and pathogenesis.

关键词： stromelysin-3 laminin receptor matrix metalloproteinase extracellular matrix Xenopus laevis cell surface substrate.

Plastins regulate ectoplasmic specialization via its actin bundling activity on microfilaments in the rat testis

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Asian Journal of Andrology 2016年第5期18卷 716-722页

作者： Nan Li Chris KC Wong C Yan Cheng The Mary M. Wohlford Laboratory for Male Contraceptive Research Center for Biomedical Research Population Council 1230 York Avenue New York 10065 USA Department of Biology Hong Kong Baptist University Hong Kong China

Plastins are a family of actin binding proteins （ABPs） known to cross-link actin microfilaments in mammalian cells, creating actin microfilament bundles necessary to confer cell polarity and cell shape. Plastins also support cell movement in response to changes in environment, involved in cell/tissue growth and development. They also confer plasticity to cells and tissues in response to infection or other pathological conditions （e.g., inflammation）. In the testis, the cell-cell anchoring junction unique to the testis that is found at the Sertoli cell-cell interface at the blood-testis barrier （BTB） and at the Sertoli-spermatid （e.g., 8-19 spermatids in the rat testis） is the basal and the apical ectoplasmic specialization （ES）, respectively. The ES is an F-actin-rich anchoring junction constituted most notably by actin microfilament bundles. A recent report using RNAi that specifically knocks down plastin 3 has yielded some insightful information regarding the mechanism by which plastin 3 regulates the status of actin microfilament bundles at the ES via its intrinsic actin filament bundling activity. Herein, we provide a brief review on the role of plastins in the testis in light of this report, which together with recent findings in the field, we propose a likely model by which plastins regulate ES function during the epithelial cycle of sDermatogenesis via their intrinsic activity on actin microfilament organization in the rat testis.

关键词： actin binding proteins actin bundling proteins cytoskeleton F-actin fimbrins plastins seminiferous epithelial cycle spermatogenesis testis

Spatial and temporal regulation of collagenases-3, -4,and stromelysin -3 implicates distinct functions in apoptosis and tissue remodeling during frog metamorphosis

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Cell Research 1999年第2期9卷 91-105页

作者： DAMJANOVSKI SASHKO ATSUKO ISHIZUYAOKA YUN-BO SHI (Laboratory of Molecular Embryology, Building 18T, Rm. 106, national institute of child health and human development, national institutes of health, Bethesda, MD, 20892, USA)(Department Of Histology and Laboratory of Molecular Embryology Building 18T Rm. 106 National Institute of Child Health and Human Development National Institutes of Health Bethesda USA Department of Histology and Neurobiology Dokkyo University School of Medicine Mibu Japan

Matrix metalloproteinases (MMPs) are a family of extracellular proteases capable of degrading various proteinaceous components of the extracellular matrix (ECM).They have been implicated to play important roles in a number of developmental and pathological processes, such as tumor metastasis and inflammation. Relatively few studies have been carried out to investigate the function of MMPs during postembryonic organ-development. Using Xenopus laevis development as a model system, we demonstrate here that three MMPs, stromelysin-3 (ST3),collagenases-3 (Col3), and Col4, have distinct spatial and temporal expression profiles during metamorphosis as the tadpole transforms into a frog. In situ hybridizations reveal a tight, but distinct, association of individual MMPs with tissue remodeling in the tail and intestine during metamorphosis. In particular, ST3 expression is strongly correlated with apoptosis in both organs as demonstrated by analyses of serial sections with in situ hybridization for ST3 mRNA and TUNEL (terminal deoxyribonucleotidyl transferase-mediated dUTP-biotin nick end labeling) for apoptosis, respectively. On the other hand, Col3 and Col4 MMPs in Xenopus laevis development are present in regions where extensive connective tissue remodeling take place. These results indicate that ST3 is likely to play a role in ECM-remodeling that facilitateapoptotic tissue remodeling or resorption while Col3 and Col4 appear to participate in connective tissue degradation during development.

关键词： Apoptosis thyroid hormone matrix metalloproteinase extracellular matrix (ECM) amphibian

Transgenic technologies for the study of epididymal function

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Asian Journal of Andrology 2000年第1期2卷 33-38页

作者： R.JohnLye BarryT.Hinton Department of Cell Biology University of Virginia Health System School of Medicine Charlotesville VA 22908 USADepartment of Cell Biology University of Virginia Health System School of Medicine Charlotesville VA 22908 USA

Sperm mature and acquire the capacity for fertilization during their transit through the epididymis, however little isknown of the molecular events that comprise sperm maturation. Recent advances in transgenic mouse technology holdpromise for illumination of this process. Most of the existing infertile, transgenic mouse lines seem to have defects inepithelial structure or sperm transport rather than direct defects in the maturation of sperm. Temporally and spatially re-stricted targeted disruptions of epididymal specific genes should provide great insight into the epididymal contribution tosperm maturation. (Asian J Androl 2000; 2: 33 - 38 )

关键词： epididymis sperm maturation transgenic organisms fertility

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Characterization and functions of beta defensins in the epididymis

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Asian Journal of Andrology 2007年第4期9卷 453-462页

作者： Susan H. Hall Suresh Yenugu Yashwanth Radhakrishnan Maria Christina W. Avellar Peter Petrusz Frank S. French Laboratories for Reproductive Biology University of North Carolina at Chapel Hill NC 27599-7505 USA Department of Biochemistry and Molecular Biology Pondicherry Central University Pondicherry 605014 India Section of Experimental Endocrinology Department of Pharmacology Universidade Federal de Sao Paulo SP 04044-020 Brazil

The epididymal β-defensins have evolved by repeated gene duplication and divergence to encode a family of proteins that provide direct protection against pathogens and also support the male reproductive tract in its primary function. Male tract defensins also facilitate recovery from pathogen attack. The β-defensins possess ancient conserved sequence and structural features widespread in multi-cellular organisms, suggesting fundamental roles in species survival. Primate SPAG11, the functional fusion of two ancestrally independent β-defensin genes, produces a large family of alternatively spliced transcripts that are expressed according to tissue-specific and species-specific constraints. The complexity of SPAG11 varies in different branches of mammalian evolution. Interactions of human SPAG11D with host proteins indicate involvement in multiple signaling pathways. （Asian J Andro12007 July; 9： 453- 462）

关键词： defensin antibacterial male fertility

Distinct expression profiles of transcriptional coactivators for thyroid hormone receptors during Xenopus laevis metamorphosis

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Cell Research 2003年第6期13卷 459-464页

作者： BINDU D PAUL national institutes of health Laboratory of Gene Regulation and development national institute of child health and human development Bldg. USA.

The biological effects of thyroid hormone (T3) are mediated by the thyroid hormone receptor (TR). Amphibian metamorphosis is one of the most dramatic processes that are dependent on T3. T3 regulates a series of orchestrated developmental changes, which ultimately result in the conversion of an aquatic herbivorous tadpole to a terrestrial carnivorous frog. T3 is presumed to bind to TRs, which in turn recruit coactivators, leading to gene activation. The best-studied coactivators belong to the p160 or SRC family. Members of this family include SRC1/ NCoA-1, SRC2/TIF2/GRIP1, and SRC3/pCIP/ACTR/AIB-l/RAC-3/TRAM-1. These SRCs interact directly with liganded TR and function as adapter molecules to recruit other coactivators such as p300/CBP. Here, we studied the expression patterns of these coactivators during various stages of development. Amongst the coactivators cloned in Xenopus laevis, SRC3 was found to be dramatically upregulated during natural and T3-induced metamorphosis, and SRC2 and p300 are express

关键词： transcription coactivators thyroid hormone receptor Xenopus laevis metamorphosis histone acetylation.