Biomedical subjects

Luisa Herrera

Publications and source records attributed to Luisa Herrera.

4 recordsLinked to original sources

PubMed2006

Adrenalectomy promotes a permanent decrease of plasma corticoid levels and a transient increase of apoptosis and the expression of Transforming Growth Factor beta1 (TGF-beta1) in hippocampus: effect of a TGF-beta1 oligo-antisense.

BACKGROUND: Corticosterone reduction produced by adrenalectomy (ADX) induces apoptosis in dentate gyrus (DG) of the hippocampus, an effect related to an increase in the expression of the pro-apoptotic gene bax. However it has been reported that there is also an increase of the anti-apoptotic gene bcl-2, suggesting the promotion of a neuroprotective phenomenon, perhaps related to the expression of transforming growth factor beta1 (TGF-beta1). Thus, we have investigated whether TGF-beta1 levels are induced by ADX, and whether apoptosis is increased by blocking the expression of TGF-beta1 with an antisense oligonucleotide (ASO) administered intracerebrally in corticosterone depleted rats. RESULTS: It was observed an increase of apoptosis in DG, 2 and 5 days after ADX, in agreement with a reduction of corticosterone levels. However, the effect of ADX on the number of apoptotic positive cells in DG was decreased 5 days after the lesion. In CA1-CA3 regions, the effect was only observed 2 days after ADX. TGF-beta1 mRNA levels were increased 2 days after ADX. The sustained intracerebro-ventricular administration of a TGF-beta1 ASO via an osmotic mini pump increased apoptosis levels in CA and DG regions 5 days after ADX as well as sham-operated control animals. No significant effect was observed following a scrambled-oligodeoxynucleotide treatment. CONCLUSION: The changes in both the pattern and the magnitude of apoptotic-cell morphology observed 2 and 5 days after ADX suggest that, as a consequence of the reduction of corticosteroids, some trophic mechanisms restricting cell death to a particular time window are elicited. Sustained intracerebral administration of TGF-beta1 ASO increased the apoptosis promoted by ADX, suggesting that TGF-beta1 plays an anti-apoptotic role in vivo in hippocampus.

Adrenalectomy↗

PubMed2006

NOD2/CARD15 and Toll-like 4 receptor gene polymorphism in Chilean patients with inflammatory bowel disease.

Crohn's disease (CD) and ulcerative colitis (UC) are multifactorial diseases with a genetic background. Genes related to the innate immune response have been observed to be involved. Polymorphisms of Toll-like receptor 4 (TLR4) and CARD15/NOD2 are thought to be involved in the pathogenesis of inflammatory bowel disease (IBD). There is no information about the frequency of these polymorphisms in South American and Chilean populations. Aim. To investigate the distribution of CARD15/NOD2 (Arg702Trp, Gly908Arg and Leu1007fsinsC) and TLR4 (Asp299Gly) polymorphisms in Chilean patients with IBD. Methods. DNA was obtained from 22 CD, 22 UC patients and 20 healthy individuals. Genotyping was performed by allele-specific PCR and by PCR-RFLP analysis. Clinical and demographic features were characterized. Results. Among the CD patients, the clinical pattern was deemed inflammatory in 14, while five had penetrating and five stricturing, variants. One patient had esophageal involvement, five perianal, seven ileal and in 16 the colon was involved. Among the UC patients, two had proctitis, two proctosigmoiditis, four left-sided colitis and 14 pancolitis. NOD2/CARD15 analysis revealed the presence of the 702Trp allele in two CD patients (both heterozygotes), 1007fsinsC in one CD patient (heterozygote) while 908Arg was found in one UC patient. The 299Gly TLR4 allele was identified in one UC and one CD patient. Conclusion. This genetic study shows that the alleles frequently associated with IBD (1007fsinsC, 908Arg and 702Trp in NOD2/CARD15 and 299Gly TLR4) have a low incidence in Chilean, IBD patients, which is similar to European populations. It is possible that, in addition to environmental factors, other genetic polymorphisms may be involved in the pathogenesis of the disease in Chilean, IBD patients.

Chile↗

PubMed2005

Mouse ovary developmental RNA and protein markers from gene expression profiling.

To identify genes involved in morphogenetic events during mouse ovary development, we started with microarray analyses of whole organ RNA. Transcripts for 60% of the 15,000 gene NIA panel were detected, and about 2000 were differentially expressed in nascent newborn compared to adult ovary. Highly differentially expressed transcripts included noncoding RNAs and newly detected genes involved in transcription regulation and signal transduction. The phased pattern of newborn mouse ovary differentiation allowed us to (1) extend information on activity and stage specificity of cell type-specific genes; and (2) generate a list of candidate genes involved in primordial follicle formation, including podocalyxin (Podxl), PDGFR-beta, and a follistatin-domain-encoding gene Flst1. Oocyte-specific transcripts included many (e.g., Deltex2, Bicd2, and Zfp37) enriched in growing oocytes, as well as a novel family of untranslated RNA's (RLTR10) that is selectively expressed in early stage follicles. The results indicate that global expression profiling of whole organ RNA provides sensitive first-line information about ovarian histogenesis for which no in vitro cell models are currently available.

Animals↗

PubMed2002

Genes and translocations involved in POF.

Changes at a single autosomal locus and many X-linked loci have been implicated in women with gonadal dysgenesis [premature ovarian failure (POF) with deficits in ovarian follicles]. For the chromosome 3 locus, a forkhead transcription factor gene (FOXL2) has been identified, in which lesions result in decreased follicles by haploinsufficiency. In contrast, sporadic X; autosomal translocations are distributed at many points on the X, but concentrate in a critical region on Xq. The association of the breakpoints with genes involved in ovarian function is thus far weak (in four analyzed cases) and has not been related to pathology in other POF patients. While many more translocations can be analyzed in detail as the human genome sequence is refined, it remains possible that translocations like X monosomy (Turner syndrome) lead to POF not by interrupting specific genes important in ovarian development, but by causing aberrations in pairing or X-inactivation during folliculogenesis. It is noted that the critical region has unusual features, neighboring the X-inactivation center and including an 18 Mb region of very low recombination. These suggest that chromosome dynamics in the region may be sensitive to structural changes, and when modified by translocations might provoke apoptosis at meiotic checkpoints. Choices among models for the etiology of POF should be feasible based on studies of ovarian follicle development and attrition in mouse models. Studies would prominently include gene expression profiling of developmental-specific pathways in nascent ovaries with controlled levels of Foxl2 and interacting proteins, or with defined changes in the X chromosome.

Chromosomes, Human, X↗