Background: The chicken embryo is an important model organism for developmental biology studies. At present, many techniques on this model have been set up, from surgical procedures to molecular biology methods, to answer capital questions of cell biology. The study of the genes involved in motoneurons (MNs) survival and cell death is critical for a better understanding of the molecular mechanisms leading to MNs degenerative diseases, such as amyothophic lateral sclerosis (ALS) and motor peripheral neuropathies.
New Method: Here, we describe the combination of a well known surgical procedure able to induce MNs cell death, the limb-bud removal (LBR), with a very popular method used in molecular biology to test gene function in living organisms, the in ovo electroporation (IOE). The aim of this work is to provide an effective method for the investigation of genes involved in MNs survival and cell death under lesion conditions.
Results: Our method allows the successful electroporation of the 40-50% of MNs on the side of LBR with a high survival rate early and late after procedure.
Comparison With Other Methods: This modified LBR technique combined with IOE allows a higher MN expression efficiency compared to an already published method.
Conclusions: Our work opens the possibility of screening a multitude of genes involved in MNs survival or cell death in vivo with high reproducibility and efficiency on a flexible and inexpensive animal model. The LBR/IOE technique opens a new way for the optimization of subsequent studies on mammalian models of diseases affecting MNs survival.
Download full-text PDF |
Source |
|---|---|
| http://dx.doi.org/10.1016/j.jneumeth.2014.10.022 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Lysophosphatidylcholine induces ceramide synthase-2 expression in primary culture model of astrocytopathy: potential therapeutic target in multiple sclerosis.
Mol Biol Rep
January 2025
Department of Pharmacology, School of Health Sciences, Central University of Punjab, Bathinda, 151401, India.
Background: Multiple sclerosis (MS) is a chronic autoimmune condition that damages the myelin sheath of neurons in the central nervous system, resulting in compromised nerve transmission and motor impairment. The astrocytopathy is considered one of the prominent etiological factor in the pathophysiology of demyelination in MS. The expression level of ceramide synthase-2 (CS-2) is yet to be established in the pathophysiology of astrocytopathy although the derailed ceramide biosynthetic pathways is well demonstrated in the pathophysiology of demyelination.
View Article and Find Full Text PDFAlcohol drinking leads to sex-dependent differentiation of T cells.
Eur J Trauma Emerg Surg
January 2025
Department of Trauma Surgery and Orthopedics, Goethe University, University Hospital, Frankfurt, Germany.
Objective: Global per capita alcohol consumption is increasing, posing significant socioeconomic and medical challenges also due to alcohol-related traumatic injuries but also its biological effects. Trauma as a leading cause of death in young adults, is often associated with an increased risk of complications, such as sepsis and multiple organ failure, due to immunological imbalances. Regulatory T cells play a crucial role in maintaining immune homeostasis by regulating the inflammatory response.
View Article and Find Full Text PDFASIC1a mediated nucleus pulposus cells pyroptosis and glycolytic crosstalk as a molecular basis for intervertebral disc degeneration.
Inflamm Res
January 2025
Department of Orthopedics and Traumatology, The Affiliated Traditional Chinese Medicine Hospital, Southwest Medical University, Luzhou, Sichuan Province, China.
Background: One of the etiologic components of degenerative spinal illnesses is intervertebral disc degeneration (IVDD), and the accompanying lower back pain is progressively turning into a significant public health problem. Important pathologic characteristics of IVDD include inflammation and acidic microenvironment, albeit it is unclear how these factors contribute to the disease.
Purpose: To clarify the functions of inflammation and the acidic environment in IVDD, identify the critical connections facilitating glycolytic crosstalk and nucleus pulposus cells (NPCs) pyroptosis, and offer novel approaches to IVDD prevention and therapy.
Age-related p53 SUMOylation accelerates senescence and tau pathology in Alzheimer's disease.
Cell Death Differ
January 2025
Department of Pathophysiology, School of Basic Medicine, Key Laboratory of Education Ministry/Hubei Province of China for Neurological Disorders, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Aging is a major risk factor for Alzheimer's disease (AD). With the prevalence of AD increased, a mechanistic linkage between aging and the pathogenesis of AD needs to be further addressed. Here, we report that a small ubiquitin-related modifier (SUMO) modification of p53 is implicated in the process which remarkably increased in AD patient's brain.
View Article and Find Full Text PDFAge-dependent differences in breast tumor microenvironment: challenges and opportunities for efficacy studies in preclinical models.
Cell Death Differ
January 2025
Laboratory of Hematology-Oncology, European Institute of Oncology IRCCS, Via Ripamonti 435, 20141, Milan, Italy.
Immunity suffers a function deficit during aging, and the incidence of cancer is increased in the elderly. However, most cancer models employ young mice, which are poorly representative of adult cancer patients. We have previously reported that Triple-Therapy (TT), involving antigen-presenting-cell activation by vinorelbine and generation of TCF1-stem-cell-like T cells (scTs) by cyclophosphamide significantly improved anti-PD-1 efficacy in anti-PD1-resistant models like Triple-Negative Breast Cancer (TNBC) and Non-Hodgkin's Lymphoma (NHL), due to T-cell-mediated tumor killing.
View Article and Find Full Text PDFWant AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!