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Blood. 2002 Nov 15;100(10):3672-80. Epub 2002 Jul 05.
Relationships between early B- and NK-lineage lymphocyte precursors in bone marrow.

Kouro T, Kumar V, Kincade PW.

Immunobiology and Cancer Program, Oklahoma Medical Research Foundation, Oklahoma City 73104, USA.

Recent studies have demonstrated that lineage marker-negative (Lin(-)) c-kit(Lo) Flk-2/Flt3(+) IL-7R(+) Sca-1(Lo) CD27(+) Ly-6C(-) Thy-1(-)CD43(+) CD16/32(Lo/-) terminal deoxynucleotidyl transferase (TdT)(+) cells in murine bone marrow are functional lymphocyte precursors. However, it has not been clear if this is an obligate intermediate step for transit of multipotential hematopoietic stem cells to natural killer (NK) cells. We have now used serum-free, stromal cell-free cultures to determine that NK progenitors are enriched among an estrogen-regulated, c-kit(Lo) subset of the Lin(-) fraction. However, several experimental approaches suggested that this population is heterogeneous and likely represents a stage where B and NK lineages diverge. Although most B-cell precursors were directly sensitive to estrogen in culture, much of the NK-cell precursor activity in that fraction was hormone resistant. B-lineage potential was largely associated with interleukin 7 receptor alpha (IL-7R(alpha)) expression and was selectively driven in culture by IL-7. In contrast, many NK precursors did not display detectable amounts of this receptor and their maturation was selectively supported by IL-15. Finally, single-cell experiments showed that the Lin(-) c-kit(Lo) fraction contains a mixture of B/NK, B-restricted, and NK-restricted progenitors. Two-step culture experiments revealed that NK precursors become hormone resistant on or before acquisition of CD122, signaling commitment to the NK lineage. CD45R is preferentially, but not exclusively, expressed on maturing B-lineage cells. Production of these 2 blood cell types is regulated in bone marrow by common and then independent mechanisms that can now be studied with greater precision.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12393656&dopt=Abstract

J Clin Invest. 2002 Oct;110(8):1093-103.
Beneficial effects of leptin on obesity, T cell hyporesponsiveness, and neuroendocrine/metabolic dysfunction of human congenital leptin deficiency.

Farooqi IS, Matarese G, Lord GM, Keogh JM, Lawrence E, Agwu C, Sanna V, Jebb SA, Perna F, Fontana S, Lechler RI, DePaoli AM, O'Rahilly S.

University Department of Medicine, Department of Clinical Biochemistry, Addenbrooke's Hospital, Cambridge, United Kingdom. afarooqgmp.mrc.ac.uk

The wide range of phenotypic abnormalities seen in the leptin-deficient ob/ob mouse and their reversibility by leptin administration provide compelling evidence for the existence of multiple physiological functions of this hormone in rodents. In contrast, information regarding the roles of this hormone in humans is limited. Three morbidly obese children, who were congenitally deficient in leptin, were treated with daily subcutaneous injections of recombinant human leptin for up to 4 years with sustained, beneficial effects on appetite, fat mass, hyperinsulinemia, and hyperlipidemia. Leptin therapy resulted in a rapid and sustained increase in plasma thyroid hormone levels and, through its age-dependent effects on gonadotropin secretion, facilitated appropriately timed pubertal development. Leptin deficiency was associated with reduced numbers of circulating CD4(+) T cells and impaired T cell proliferation and cytokine release, all of which were reversed by recombinant human leptin administration. The subcutaneous administration of recombinant human leptin has major and sustained beneficial effects on the multiple phenotypic abnormalities associated with congenital human leptin deficiency.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12393845&dopt=Abstract

J Biol Chem. 2002 Dec 27;277(52):50422-30. Epub 2002 Oct 21.
Homo- and hetero-oligomerization of thyrotropin-releasing hormone (TRH) receptor subtypes. Differential regulation of beta-arrestins 1 and 2.

Hanyaloglu AC, Seeber RM, Kohout TA, Lefkowitz RJ, Eidne KA.

7TM Receptor Laboratory, Western Australian Institute for Medical Research (WAIMR), University of Western Australia, Centre for Medical Research, Nedlands, Perth, WA 6009, Australia.

G-protein-coupled receptors (GPCRs) are regulated by a complex network of mechanisms such as oligomerization and internalization. Using the GPCR subtypes for thyrotropin-releasing hormone (TRHR1 and TRHR2), the aim of this study was to determine if subtype-specific differences exist in the trafficking process. If so, we wished to determine the impact of homo- and hetero-oligomerization on TRHR subtype trafficking as a potential mechanism for the differential cellular responses induced by TRH. Expression of either beta-arrestin 1 or 2 promoted TRHR1 internalization. In contrast, only beta-arrestin 2 could enhance TRHR2 internalization. The preference for beta-arrestin 2 by TRHR2 was supported by the impairment of TRHR2 trafficking in mouse embryonic fibroblasts (MEFs) from either a beta-arrestin 2 knockout or a beta-arrestin 1/2 knockout, while TRHR1 trafficking was only abolished in MEFs lacking both beta-arrestins. The differential beta-arrestin-dependence of TRHR2 was directly measured in live cells using bioluminescence resonance energy transfer (BRET). Both BRET and confocal microscopy were also used to demonstrate that TRHR subtypes form hetero-oligomers. In addition, these hetero-oligomers have altered internalization kinetics compared with the homo-oligomer. The formation of TRHR1/2 heteromeric complexes increased the interaction between TRHR2 and beta-arrestin 1. This may be due to conformational differences between TRHR1/2 hetero-oligomers versus TRHR2 homo-oligomers as a mutant TRHR1 (TRHR1 C335Stop) that does not interact with beta-arrestins, could also enhance TRHR2/beta-arrestin 1 interaction. This study demonstrates that TRHR subtypes are differentially regulated by the beta-arrestins and also provides the first evidence that the interactions of TRHRs with beta-arrestin may be altered by hetero-oligomer formation.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12393857&dopt=Abstract

J Biol Chem. 2003 Jan 3;278(1):104-10. Epub 2002 Oct 19.
Natural structural variants of the nuclear receptor farnesoid X receptor affect transcriptional activation.

Zhang Y, Kast-Woelbern HR, Edwards PA.

Department of Biological Chemistry, University of California, Los Angeles, California 90095, USA.

The Farnesoid X receptor (FXR) is a member of the nuclear hormone receptor superfamily that has been shown to play an important role in bile acid and cholesterol homeostasis. Here we identify four murine FXR transcripts, derived from a single gene, that encode four isoforms, FXRalpha1, FXRalpha2, FXRbeta1, and FXRbeta2. FXRalpha and FXRbeta differ at their amino terminus, and FXRalpha1 and FXRbeta1 have a four-amino acid residue insertion in the hinge region immediately adjacent to the DNA binding domain. Real time PCR and 5'-rapid amplification of cDNA ends followed by Southern blotting reveal that these four transcripts are expressed differentially in liver, intestine, kidney, adrenals, stomach, fat, and heart. Electrophoretic mobility shift assays demonstrate that FXRalpha2 and FXRbeta2 bind to FXR response elements with a higher affinity as compared with FXRalpha1 and FXRbeta1, suggesting that the four-amino acid insert may affect FXR function. Consistent with this idea, the results of transient transfection experiments demonstrate that the four FXR isoforms differentially transactivated a number of promoter-reporter genes; activation of an ileal bile acid-binding protein promoter-reporter gene varied 20-fold depending on the FXR isoform; the rank order of activation was FXRbeta2 > FXRalpha2 FXRalpha1 = FXRbeta1. In contrast, SHP reporter or BSEP reporter genes were activated to similar degrees by each of the FXR isoforms. Finally, NIH3T3 cells were stably infected with individual murine FXR isoforms, and the cells were treated with FXR ligands. The endogenous ileal bile acid-binding protein gene was activated by the four FXR isoforms with the same rank order as seen in transfections. This effect was gene-specific, since induction of bile salt export pump mRNA was independent of the FXR isoform. These observations suggest that there are four distinct murine FXR isoforms that differentially regulate gene expression in numerous tissues in vivo.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12393883&dopt=Abstract

Mol Med. 2002 Jul;8(7):367-75.
Differential regulation of functional gene clusters in overt coronary artery disease in a transgenic atherosclerosis-hypertensive rat model.

Herrera VM, Didishvili T, Lopez LV, Ruiz-Opazo N.

Unit of Molecular Genetics, Whitaker Cardiovascular Institute, Section of Molecular Medicine, Evans Department of Medicine, Boston University School of Medicine, Boston, MA 02118, USA. vherreru.edu

BACKGROUND: Human acute coronary syndrome refers to the spectrum of clinical manifestations of overt coronary artery (CAD) disease characterized by atherosclerotic plaque destabilization and resultant myocardial injury. Typically studied as distinct pathologies, emerging pathogenic paradigms implicate multiple processes beyond thrombosis and ischemic cell injury respectively, with significant pathway overlap involving inflammation, apoptosis, matrix degradation, and oxidative stress. However, all these pathways have also been implicated in still-quiescent coronary plaque progression, thus making it harder to pinpoint the turnkey events leading to overt-CAD. Analysis of transcription profiles could identify a working framework of pathogenesis distinguishing overt-CAD. MATERIALS AND METHODS: We investigated the transcription profile associated with overt-coronary artery disease (CAD), in contrast to quiescent-CAD and attenuated, quiescent-CAD using the Tg 53 transgenic atherosclerosis-hypertensive rat model, which exhibits end-stage coronary heart disease simulating human acute coronary syndromes. Using a rat-specific known-gene oligonucleotide array, twice corroborated transcription profiles from four individual Tg 53 rats exhibiting overt-CAD were analyzed and contrasted to transcription profiles of age-matched Tg 53 rats with quiescent-CAD (pooled n = 4) and attenuated, quiescent-CAD (pooled n = 4). RESULTS: Tg 53 male rats with overt-CAD exhibited distinct transcription profiles compared with both quiescent-CAD control groups. Functional gene cluster analysis detects upregulation of genes involved in inflammation (interleukin-1, interleukin-18, Fc gamma II receptor, thyrotropin releasing hormone), matrix balance (membrane type metalloproteinase, TIMP-1, lysyl oxidase), oxidized LDL entry (endothelial oxLDL receptor), which contrast deinduced gene clusters involved in angiogenesis, proliferation, metabolism, ion transport and adrenergic receptors. CONCLUSION: The data demonstrate that transcriptionally mediated events distinguish the onset of overt-CAD and identify a first list of putative "turnkey" genes. This altered molecular framework implies an altered "hardwiring" which a priori would require multifaceted, targeted intervention- currently not implemented to date. Although more studies are necessary, early concordance with current pathogenic paradigms of human coronary plaque destabilization and post-ischemic myocardial response provides translational significance to observations and hypotheses.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12393934&dopt=Abstract

The average human scalp is covered by approximatey 100,000 hair follicles. Each hair undergoes hair cycle and normally 50-100 hairs randomly fall out a day, which is unnoticeable because lost hair is replaced by as many new hairs springing up daily. Hair loss results from the fall out of hair from the hair follicle. Alopecia or excessive, premature hair loss is the condition caused by many factors. Loss of hair itself does not pose critical health problems because biological role of human hair is relatively marginal. Hair on our scalp protects the head from mechanical shock, heat loss, and exposure to UV-light. The eyelashes and eyebrowes protect the eyes, and hair in the ear canal or the nasal passages help filter out particles and pathogens, thus protecting our internal organs. However, hair does play important social role: it is one of the major determinants of our appearance and identity in daily life. Fullness of hair also implicates or manifests physical integrity and youthfulness of the person. Losing hair could have more than just emotional impacts on individuals. The hair is a unique organ that goes through a characteristic cycle consisting of an immature phase, a growing phase called anagen, a transitional phase between the growing phase and the resting phase called catagen, and finally a resting phase called telogen in which the hair stops growing, waiting to fall out. 85-90% of hairs on our body are in anagen phase or growing phase, which lasts anywhere from two to five years. This phase is followed by a short regression phase, or catagen, which lasts 2-3 weeks. Approximately 1% of hair follicles are in catagen. Approximately 10-15% of hair follicles are in the resting phase, the telogen, which lasts about 3-5 months. Hair follicles typically goes through 10-20 asynchronous cycles during the lifetime. Persistent loss of more than 150 hairs would consist a state of hair loss, or alopecia, albeit it could be temporary.

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