Rajesh C. Miranda

ORCID: 0000-0002-8359-892X
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About
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Research Areas
  • Prenatal Substance Exposure Effects
  • Birth, Development, and Health
  • Pregnancy and preeclampsia studies
  • MicroRNA in disease regulation
  • Epigenetics and DNA Methylation
  • Neurogenesis and neuroplasticity mechanisms
  • Neonatal and fetal brain pathology
  • Cancer-related molecular mechanisms research
  • Spinal Cord Injury Research
  • Nerve injury and regeneration
  • Fatty Acid Research and Health
  • Estrogen and related hormone effects
  • Neuroscience and Neuropharmacology Research
  • RNA modifications and cancer
  • Pain Mechanisms and Treatments
  • Circular RNAs in diseases
  • Gestational Diabetes Research and Management
  • RNA Research and Splicing
  • Folate and B Vitamins Research
  • Neuroscience of respiration and sleep
  • Neuroinflammation and Neurodegeneration Mechanisms
  • Cancer-related gene regulation
  • Glaucoma and retinal disorders
  • Renal and Vascular Pathologies
  • Optical Imaging and Spectroscopy Techniques

Texas A&M University
2016-2025

Texas A&M Health Science Center
2015-2024

Bryan College
2015-2023

Florida College
2021

University of Florida
2021

Hospital Israelita Albert Einstein
2019

Charité - Universitätsmedizin Berlin
2012

The University of Texas at Austin
2010

Rush University Medical Center
2010

National Institute on Alcohol Abuse and Alcoholism
2010

We have been studying the role and mechanism of estrogen action in survival differentiation neurons basal forebrain its targets cerebral cortex, hippocampus, olfactory bulb. Previous work has shown that estrogen-target these regions widely coexpress mRNAs for neurotrophin ligands their receptors, suggesting a potential substrate estrogen-neurotrophin interactions. Subsequent indicated regulates expression two receptor prototypic peripheral neural nerve growth factor. report herein gene...

10.1073/pnas.92.24.11110 article EN Proceedings of the National Academy of Sciences 1995-11-21

The rodent and primate basal forebrain is a target of family endogenous peptide signaling molecules, the neurotrophins--nerve growth factor, brain-derived neurotrophic neurotrophin 3--and gonadal steroid hormone estrogen, both which have been implicated in cholinergic function. To investigate whether or not these ligands may act on same neurons developing adult forebrain, we combined autoradiography with 125I-labeled estrogen either nonisotopic situ hybridization histochemistry...

10.1073/pnas.89.10.4668 article EN Proceedings of the National Academy of Sciences 1992-05-15

We previously showed that middle-aged female rats sustain a larger infarct following experimental stroke as compared to younger rats, and paradoxically, estrogen treatment the older group is neurotoxic. Plasma brain insulin-like growth factor-1 (IGF-1) levels decrease with age. However, IGF-1 infusion stroke, prevents neurotoxicity in rats. IGF1 neuroprotective well tolerated, but also has potentially undesirable side effects. hypothesized microRNAs (miRNAs) target signaling family for...

10.1371/journal.pone.0032662 article EN cc-by PLoS ONE 2012-02-29

The fetal brain is sensitive to a variety of teratogens, including ethanol. We showed previously that ethanol induced mitosis and stem cell maturation, but not death, in cerebral cortex-derived progenitors. tested the hypothesis micro-RNAs (miRNAs) could mediate teratogenic effects mouse neurosphere culture model. Ethanol, at level attained by alcoholics, significantly suppressed expression four miRNAs, miR-21, -335, -9, -153, whereas lower concentration, attainable during social drinking,...

10.1523/jneurosci.1269-07.2007 article EN cc-by-nc-sa Journal of Neuroscience 2007-08-08

Development and survival of neurons in the central nervous system are dependent on activity a variety endogenous neurotrophic agents. Using combined isotopic nonisotopic situ hybridization histochemistry, we have found that subsets within developing forebrain coexpress mRNAs for both neurotrophins (nerve growth factor, brain-derived neurotrophin 3) their receptors (p75NGFR, TrkA, TrkB). The colocalization mRNA ligands presumptive target suggests potential autocrine paracrine mechanisms...

10.1073/pnas.90.14.6439 article EN Proceedings of the National Academy of Sciences 1993-07-15

<h3>Abstract</h3> <h3>Background:</h3> We evaluated smell identification as a biomarker for Alzheimer disease (AD) by assessing its utility in differentiating normal aging from an amnestic disorder and determining predictive value conversion mild cognitive impairment (aMCI) to AD. <h3>Methods:</h3> Cross-sectional study (AD = 262, aMCI 110, controls 194) measuring (University of Pennsylvania Smell Identification Test [UPSIT]) status was performed, well longitudinal analysis participants (n...

10.1212/cpj.0000000000000293 article EN Neurology Clinical Practice 2017-02-01

Abstract Recent work has shown that estrogen receptor mRNA and protein co‐localize with neurotrophin systems in the developing basal forebrain. In present study we examined potential for reciprocal regulation of by their ligands a prototypical target, PC12 cell. using situ hybridization histochemistry, RT‐PCR modified nuclear exchange assay, found both binding cells. Moreover, while was relatively low naive cells, long‐term exposure to NGF enhanced these cells sixfold. Furthermore,...

10.1002/neu.480250807 article EN Journal of Neurobiology 1994-08-01

Small non-coding RNA [miRNA (microRNA)] found in the circulation have been used successfully as biomarkers and mechanistic targets for chronic acute disease. The present study investigated impact of age sex on miRNA expression following ischaemic stroke an animal model. Adult (6 month) middle-aged (11–12 months) female male rats were subject to MCAo (middle cerebral artery occlusion) using ET-1 (endothelin-1). Circulating miRNAs analysed blood samples at 2 5 days post-stroke, brain...

10.1042/cs20130565 article EN Clinical Science 2014-01-16

Background Ethanol ( EtOH ) and nicotine are often co‐abused. However, their combined effects on fetal neural development, particularly stem cells NSC s), which generate most neurons of the adult brain during second trimester pregnancy, poorly understood. We previously showed that influenced maturation in part, by suppressing expression specific micro RNA s (mi s). Here, we tested extent to coregulated known ‐sensitive R ‐9, mi ‐21, ‐153, ‐335), a nicotine‐sensitive ‐140‐3p), mRNA for...

10.1111/j.1530-0277.2012.01793.x article EN Alcoholism Clinical and Experimental Research 2012-03-28

In recent years, we have come to recognize that a multitude of in utero exposures the capacity induce development congenital and metabolic defects. As most these encounters manifest their effects beyond window exposure, deciphering mechanisms teratogenesis is incredibly difficult. For many agents, altered epigenetic programming has become suspect transmitting lasting signature exposure leading dysgenesis. However, while several chemicals can perturb chromatin structure acutely, for agents...

10.1186/s13072-015-0031-7 article EN cc-by Epigenetics & Chromatin 2015-09-28

Fetal alcohol spectrum disorders (FASD) are difficult to diagnose since many heavily exposed infants, at risk for intellectual disability, do not exhibit craniofacial dysmorphology or growth deficits. Consequently, there is a need biomarkers that predict disability. In both animal models and human studies, exposure during pregnancy resulted in significant alterations circulating microRNAs (miRNAs) maternal blood. the current study, we asked if changes plasma miRNAs alcohol-exposed pregnant...

10.1371/journal.pone.0165081 article EN cc-by PLoS ONE 2016-11-09

In animal models, middle-aged females sustain greater ischemia-induced infarction as compared to adult females. This age difference in infarct severity is associated with reduced functional capacity of astrocytes, a critical neural support cell. The impaired response astrocytes following stroke may be related epigenetic alterations, including histone acetylation or methylation. present study measured the activity enzymes that regulate and methylation cerebral cortical (6 month) (11+ female...

10.1080/15592294.2014.1001219 article EN Epigenetics 2015-02-01

Background While 2 to 5% of school‐aged children in the United States are estimated be affected by fetal alcohol spectrum disorders ( FASD ), prevalence prenatal exposure PAE ) might substantially underreported. Our objective was systematically estimate Texas measuring a direct ethanol metabolite, phosphatidylethanol PE th), 1,000 infant residual dried blood spots (ir DBS s) Newborn Screening Repository. Methods All public health regions PHR were represented proportional their 2014 birth...

10.1111/acer.13375 article EN Alcoholism Clinical and Experimental Research 2017-03-14

The developing cerebral cortex undergoes a period of substantial cell death. present studies examine the role suicide receptor Fas/Apo[apoptosis]-1 in cortical development. Fas mRNA and protein are transiently expressed subsets cells within rat during peak apoptosis. Fas-immunoreactive were localized close proximity to ligand (FasL)-expressing cells. Fas-associated signaling interacting (RIP) was by some Fas-expressing cells, whereas death domain (FADD) undetectable early postnatal cortex....

10.1523/jneurosci.19-05-01754.1999 article EN cc-by-nc-sa Journal of Neuroscience 1999-03-01

Abstract Background The fetal cortical neuroepithelium is a mosaic of distinct progenitor populations that elaborate diverse cellular fates. Ethanol induces apoptosis and interferes with the survival differentiating neurons. However, we know little about ethanol's effects on neuronal progenitors. We therefore exposed neurosphere cultures from rat cerebral cortex, to varying ethanol concentrations, examine impact stem cell fate. Results promoted cycle progression, increased number diversity...

10.1186/1471-2202-6-59 article EN cc-by BMC Neuroscience 2005-09-13

The distribution of estrogen receptor mRNA expression was studied in the developing rat cerebral cortex by situ hybridization histochemistry. We used a specific, nonisotopically (digoxigenin) labeled, synthetic oligo deoxyribonucleotide complementary to 48 base se quence region estrogen-binding domain uterine cDNA. During develop ment, observed all fore brain regions previously reported bind estrogen, as determined steroid autoradiography or nuclear ing assay. In cortex, extensively...

10.1093/cercor/2.1.1 article EN Cerebral Cortex 1992-01-01

Prior studies have shown that neurons within the spinal cord are sensitive to response-outcome relations, a form of instrumental learning. Spinally transected rats receive shock one hind leg learn maintain in flexed position minimizes net exposure (controllable shock). uncontrollable stimulation (intermittent shock) inhibits this spinally mediated Here it is undermines recovery function after contusion injury. Rats received moderate injury (12.5 mm drop) and was monitored for 6 weeks. In...

10.1089/neu.2004.21.1795 article EN Journal of Neurotrauma 2004-12-01

Animal studies modeling fetal alcohol syndrome have demonstrated that developmental exposure to is associated with decreased brain weight and significant neuronal loss in multiple regions of the developing brain. Our previous data suggest Fas/Apo [apoptosis]-1 receptor transiently expressed cerebral cortex during peak period naturally occurring apoptotic cell death maximum sensitivity alcohol. Therefore, we hypothesized ethanol increases expression suicide receptors such as Fas/Apo-1 leads...

10.1111/j.1530-0277.2000.tb02022.x article EN Alcoholism Clinical and Experimental Research 2000-04-01

The spatial distribution of cells in the adult rodent forebrain which express estrogen receptor mRNA, as shown by situ hybridization histochemistry with isotopically-labeled probes, has been reported to overlap regions that are known targets and bind estrogen. extent detection mRNA within developing neurons postnatal day 10–12 female rat is accompanied translation into binding sites was investigated combining [125I]estrogen autoradiography non-isotopic (digoxigenin) hybridization, using a...

10.1016/0006-8993(92)90606-a article EN cc-by-nc-nd Brain Research 1992-03-01
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