Biology subjects

Huerta, H.

Publications and source records attributed to Huerta, H..

6 recordsLinked to original sources

bioRxiv2026

An update on the mosquito fauna of Aguascalientes, Mexico: morphological and molecular identifications, host-feeding patterns, and the removal of Aedes idahoensis (Theobald) from Mexico

To better understand taxonomic identity and feeding patterns of mosquitoes in all physiographic regions and sub-regions of Aguascalientes, Mexico, we conducted surveillance followed by morphologic analysis and DNA metabarcoding. We targeted the Sierra Madre Occidental, Central Plateau, and Neo-Volcanic Axis. We sampled natural larval habitat for immature stages and adults were collected using Shannon and CDC light traps, mechanical aspirators, and human landing catch method. In addition, curated specimens from Aguascalientes deposited in a local institution were re-examined. Overall, 5,227 mosquito specimens consisting of 357 larvae, 199 larval exuviae, 373 pupal exuviae, 33 pupae, 3,000 females, 1,264 males, and 1 male genitalia were examined using taxonomic keys. Most immature and adult species (n = 20/34 species representing 58.8% coverage) were barcoded for molecular species designation, and a subsample (n = 64) of engorged female mosquitoes were analyzed for blood feeding patterns. Two subfamilies, four tribes, seven genera, 14 subgenera, and 34 species were identified, which one tribe, three genera, nine subgenera, and 22 species are new records. Phylogenetic analysis of specimens from Aguascalientes identified 20 species. Morphological observation of mosquitoes deposited in entomological collections resulted in the removal of Aedesidahoensis from Mexico, leaving the country with a total of 255 species documented. Bloodmeal metabarcoding was successful in 23 mosquitoes of five species, revealing evidence of feeding on more than a single vertebrate species in 17 individuals. Birds were the most common host with the cattle egret (Ardea ibis) found in 18 out of 23 mosquitoes. This update on the taxonomic identity and mosquito richness and feeding patterns from Aguascalientes affords a better understanding of the ecology of medically important mosquito species.

zoology↗

bioRxiv2025

Urban Establishment of Aedes vittatus in Yucatan, Mexico

Aedes vittatus, an invasive mosquito competent for multiple arboviruses, has expanded far beyond its historical range. We report its first detection and urban establishment in mainland Americas, in Merida, Mexico. This underscores the urgent need to strengthen surveillance, risk assessment, and preparedness against invasive Aedes species across the region.

zoology↗

bioRxiv2024

Calcium (Ca2+) fluxes at Mitochondria-ER Contact Sites (MERCS) are a new target of senolysis in Therapy-Induced Senescence (TIS).

O_LIThis study investigates the state of calcium (Ca2+) flux and Mitochondria-ER contact sites (MERCS) on Therapy-Induced Senescence (TIS). C_LIO_LITIS cells-induced by Doxorubicin and Etoposide increase their MERCS contact surface but exhibit a decreased ER-mitochondria Ca2+ flux. C_LIO_LITIS cells show decreased levels of IP3R isoforms and a decreased interaction between type 1 IP3R isoform and VDAC1. C_LIO_LIThe ER-mitochondria Ca2+ flux is essential to maintain the viability of senescence cells. C_LIO_LIInhibition of ER-mitochondria Ca2+ flux rise as a new target of senolysis in vitro and in vivo. C_LI

cell biology↗

bioRxiv2023

Ketogenic diet administration later in life improves memory and regulates the synaptic cortical proteome through the cAMP/PKA signaling pathway in aging mice.

Aging is a complex biological process that compromises brain function and neuronal network activity, leading to cognitive decline and synaptic dysregulation. In recent years, a cyclic Ketogenic Diet (KD) has emerged as a potential treatment to ameliorate cognitive decline by improving memory in aged mice after long-term administration. However, the molecular mechanisms that govern such changes remains unclear. Additionally, whether short-term cyclic KD administration later in life preserves memory has not been addressed in detail. Accordingly, here we investigated how a short-term cyclic KD starting at 20-23 months-old regulates brain function of aged mice. Behavioral testing and long-term potentiation (LTP) recordings revealed that a cyclic KD improves working memory and hippocampal LTP in 24-27 months-old mice after 16 weeks of treatment. Moreover, the diet also promotes higher dendritic arborization complexity and dendritic spine density in the prefrontal cortex. Furthermore, to elucidate the molecular mechanisms underlying the memory improvements elicited by a cyclic KD, cortical synaptosomes of aged mice fed with this diet for 1 year were analyzed by mass spectrometry. Bioinformatics analysis revealed that long-term cyclic KD administration predominantly modulates the presynaptic compartment by inducing changes in the cAMP/PKA signaling pathway, the synaptic vesicle cycle, and the actin/microtubule cytoskeleton. To test these findings in vivo, synaptic proteins from cortices of 24-27-month-old mice fed with control or cyclic KD for 16 weeks were analyzed by western blot. Interestingly, increased Brain Derived Neurotrophic Factor abundance, MAP2 phosphorylation and PKA activity were observed. Overall, we show that a cyclic KD regulates brain function and memory even when it is administered at late mid-life and significantly triggers several molecular features of long-term administration, including the PKA signaling pathway and cytoskeleton dynamics, thus promoting synaptic plasticity at advanced age.

neuroscience↗

bioRxiv2021

Necroptosis inhibition counteracts axonal degeneration, cognitive decline and key hallmarks of aging, promoting brain rejuvenation.

Age is the main risk factor for the development of neurodegenerative diseases. In the aged brain, axonal degeneration is an early pathological event, preceding neuronal dysfunction, and cognitive disabilities in humans, primates, rodents, and invertebrates. Necroptosis mediates degeneration of injured axons, but whether necroptosis triggers neurodegeneration and cognitive impairment along aging is unknown. Here we show that the loss of the necroptotic effector Mlkl was sufficient to delay age-associated axonal degeneration and neuroinflammation, protecting against decreased synaptic transmission and memory decline in aged mice. Moreover, short-term pharmacologic inhibition of necroptosis in aged mice reverted structural and functional hippocampal impairment, both at the electrophysiological and behavioral level. Finally, a quantitative proteomic analysis revealed that necroptosis inhibition leads to an overall improvement of the aged hippocampal proteome, including a subclass of molecular biofunctions associated with brain rejuvenation, such as long-term potentiation and synaptic plasticity. Our results demonstrate that necroptosis contributes to the age-dependent brain degeneration, disturbing hippocampal neuronal connectivity, and cognitive function. Therefore, necroptosis inhibition constitutes a potential geroprotective strategy to treat age-related disabilities associated with memory impairment and cognitive decline.

neuroscience↗

bioRxiv2020

Control of mammalian brain aging by the unfolded protein response (UPR)

Aging is the major risk factor for the development of dementia and neurodegenerative disorders, and the aging brain manifests severe deficits in buffering capacity by the proteostasis network. Accordingly, we investigated the significance of the unfolded protein response (UPR), a major signaling pathway that copes with endoplasmic reticulum (ER) stress, to normal mammalian brain aging. Genetic disruption of ER stress sensor IRE1 accelerated cognitive and motor dysfunction during aging. Exogenous bolstering of the UPR by overexpressing an active form of the transcription factor XBP1 restored synaptic and cognitive function in addition to reducing cell senescence. Remarkably, proteomic profiling of hippocampal tissue indicated that XBP1s expression corrected age-related alterations in synaptic function. Collectively, our data demonstrate that strategies to manipulate the UPR sustain healthy brain aging. One Sentence SummaryThe IRE1/XBP1 pathway dictates when and how brain function declines during aging.

neuroscience↗