scholarly journals Cardiac neural crest cells contribute to the dormant multipotent stem cell in the mammalian heart

2005 ◽  
Vol 170 (7) ◽  
pp. 1135-1146 ◽  
Author(s):  
Yuichi Tomita ◽  
Keisuke Matsumura ◽  
Yoshio Wakamatsu ◽  
Yumi Matsuzaki ◽  
Isao Shibuya ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Neural Crest ◽  
Side Population ◽  
Side Population Cell ◽  
Multi Drug Resistance ◽  
Multipotent Stem Cells ◽  
Cardiac Neural Crest ◽  
Differentiated Cells ◽  
Undifferentiated Cells ◽  
The Right

Arodent cardiac side population cell fraction formed clonal spheroids in serum-free medium, which expressed nestin, Musashi-1, and multi-drug resistance transporter gene 1, markers of undifferentiated neural precursor cells. These markers were lost following differentiation, and were replaced by the expression of neuron-, glial-, smooth muscle cell–, or cardiomyocyte-specific proteins. Cardiosphere-derived cells transplanted into chick embryos migrated to the truncus arteriosus and cardiac outflow tract and contributed to dorsal root ganglia, spinal nerves, and aortic smooth muscle cells. Lineage studies using double transgenic mice encoding protein 0–Cre/Floxed-EGFP revealed undifferentiated and differentiated neural crest-derived cells in the fetal myocardium. Undifferentiated cells expressed GATA-binding protein 4 and nestin, but not actinin, whereas the differentiated cells were identified as cardiomyocytes. These results suggest that cardiac neural crest-derived cells migrate into the heart, remain there as dormant multipotent stem cells—and under the right conditions—differentiate into cardiomyocytes and typical neural crest-derived cells, including neurons, glia, and smooth muscle.

scholarly journals Notch2 is required for the proliferation of cardiac neural crest-derived smooth muscle cells

2008 ◽  
Vol 237 (4) ◽  
pp. 1144-1152 ◽  
Author(s):  
Prajakta Varadkar ◽  
Matthew Kraman ◽  
Daryl Despres ◽  
Ge Ma ◽  
Julie Lozier ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Neural Crest ◽  
Muscle Cells ◽  
Cardiac Neural Crest

Abstract 307: Angiotensin II Infusion Does Not Influence the Distribution of Cardiac Neural Crest Derived Smooth Muscle Cells in the Ascending Aorta

2016 ◽  
Vol 36 (suppl_1) ◽  
Author(s):  
Hisashi Sawada ◽  
Jessica J Moorleghen ◽  
Debra L Rateri ◽  
Alan Daugherty
Keyword(s):  
Smooth Muscle ◽  
Angiotensin Ii ◽  
Neural Crest ◽  
Ascending Aorta ◽  
Cell Type ◽  
Cardiac Neural Crest ◽  
Adult Mice ◽  
Embryonic Origin ◽  
Neural Crest Origin ◽  
Beta Galactosidase

Objective: Angiotensin II (Ang II) causes vascular pathology including hypertrophy and aneurysms. Smooth muscle cells (SMCs) exert a pivotal role in vascular remodeling. The localization of these vascular pathologies may be associated with distinct embryonic origins of SMCs. While there is evidence that most SMCs derive from the cardiac neural crest in the ascending aorta, other data has inferred a greater complexity of origins for this cell type. The aim of this study was to determine whether heterogeneity of the embryonic origin of SMCs in the ascending aorta is influenced by AngII. Methods and Results: ROSA26 lacZ mice were bred to mice expressing Cre under control of the Wnt1 promoter to track SMCs of cardiac neural crest origin. Gross examination of beta-galactosidase stained aortas from adult mice demonstrated cells of cardiac neural crest present from the sinotubular ascending aorta to just distal to the subclavian branch. For further examination of cell type distribution, both sagittal and cross sections were obtained. These stained sections demonstrated there was a distinct distribution on the anterior aspect of the ascending aorta, with SMCs of cardiac neural crest origin only being present in the inner laminal layers. On the proximal area of this region, there was transmural staining for beta-galactosidase. Much of the aortic arch to the subclavian branch also had transmural beta-galactosidase staining. Previous studies have demonstrated that infusion of AngII promotes pathology that varies along the length of the ascending aorta. Also, the medial pathology is most pronounced on the adventitial aspect. Therefore, we examined whether the distribution of cardiac neural crest-derived SMCs was influenced during AngII infusion. However, after 28 days of pressor infusion rates of AngII, there was no overt change in the distribution of cardiac neural crest-derived SMCs in the ascending aorta. Conclusion: SMCs from the outer aspect of the media are derived from a different embryonic origin. Cardiac neural crest derived-SMCs retain their unique distribution in the inner media of the ascending aorta during AngII infusion in adult mice.

scholarly journals Differentiation of BC3H1 smooth muscle cells changes the bivalent cation selectivity of the capacitative Ca2+ entry pathway

1996 ◽  
Vol 316 (3) ◽  
pp. 759-764 ◽  
Author(s):  
Lisa M. BROAD ◽  
David A. POWIS ◽  
Colin W. TAYLOR
Keyword(s):  
Smooth Muscle ◽  
Cell Types ◽  
Bivalent Cation ◽  
Fura 2 ◽  
Entry Pathway ◽  
Cation Selectivity ◽  
Differentiated Cells ◽  
Undifferentiated Cells ◽  
Rapid Removal ◽  
Permeation Properties

Differentiation of BC3H1 cells leads to expression of a variety of proteins characteristic of smooth muscle and to changes in the behaviour of intracellular Ca2+ stores. Treatment of both differentiated and undifferentiated cells with thapsigargin (2 μM) emptied their intracellular Ca2+ stores, and in the presence of extracellular Ca2+ caused an increase in cytosolic [Ca2+] that rapidly reversed after its removal. The amplitudes of these capacitative Ca2+ entry signals were 101±8 nM (n = 42) in differentiated cells and 188±16 nM (n = 35) in undifferentiated cells. Mn2+ entry in thapsigargin-treated cells, measured by recording the quenching of cytosolic fura 2 fluorescence, was 374±26% (n = 34) and 154±7% (n = 41) of control rates in differentiated and undifferentiated cells, respectively. Empty stores caused Ba2+ entry to increase to 282±20% (n = 8) of its basal rate in differentiated cells and to 187±20% (n = 8) in undifferentiated cells. Rates of Ca2+ extrusion, measured after rapid removal of extracellular Ca2+ from cells in which capacitative Ca2+ entry had been activated, were similar in differentiated (t½ = 23±2 s, n = 7) and undifferentiated (23±1 s, n = 6) cells. The different relationships between capacitative Ca2+ and Mn2+ signals are not, therefore, a consequence of more active Ca2+ extrusion mechanisms in differentiated cells, nor are they a consequence of different fura 2 loadings in the two cell types. We conclude that during differentiation of BC3H1 cells, the cation selectivity of the capacitative pathway changes, becoming relatively more permeable to Mn2+ and Ba2+. The change may result either from expression of a different capacitative pathway or from modification of the permeation properties of a single pathway.

scholarly journals PC12 and THP-1 Cell Lines as Neuronal and Microglia Model in Neurobiological Research

2021 ◽  
Vol 11 (9) ◽  
pp. 3729
Author(s):  
Katarzyna Balon ◽  
Benita Wiatrak
Keyword(s):  
Cell Culture ◽  
Dna Damage ◽  
Cell Lines ◽  
Inflammatory Factor ◽  
Research Model ◽  
Differentiated Cells ◽  
Undifferentiated Cells ◽  
Primary Cell Lines ◽  
Neurobiological Research ◽  
The Impact

Models based on cell cultures have become a useful tool in modern scientific research. Since primary cell lines are difficult to obtain and handle, neoplasm-derived lines like PC12 and THP-1 offer a cheap and flexible solution for neurobiological studies but require prior differentiation to serve as a neuronal or microglia model. PC12 cells constitute a suitable research model only after differentiation by incubation with nerve growth factor (NGF) and THP-1 cells after administering a differentiation factor such as phorbol 12-myristate-13-acetate (PMA). Still, quite often, studies are performed on these cancer cells without differentiation. The study aimed to assess the impact of PC12 or THP-1 cell differentiation on sensitivity to harmful factors such as Aβ25-35 (0.001–5 µM) (considered as one of the major detrimental factors in the pathophysiology of Alzheimer’s disease) or lipopolysaccharide (1–100 µM) (LPS; a pro-inflammatory factor of bacterial origin). Results showed that in most of the tests performed, the response of PC12 and THP-1 cells induced to differentiation varied significantly from the effect in undifferentiated cells. In general, differentiated cells showed greater sensitivity to harmful factors in terms of metabolic activity and DNA damage, while in the case of the free radicals, the results were heterogeneous. Obtained data emphasize the importance of proper differentiation of cell lines of neoplastic origin in neurobiological research and standardization of cell culture handling protocols to ensure reliable results.

scholarly journals The Impact of Differentiation on Cytotoxicity and Insulin Sensitivity in Streptozotocin Treated SH-SY5Y Cells

2021 ◽  
Vol 46 (6) ◽  
pp. 1350-1358
Author(s):  
Fruzsina Bagaméry ◽  
Kamilla Varga ◽  
Kitti Kecsmár ◽  
István Vincze ◽  
Éva Szökő ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Insulin Sensitivity ◽  
Insulin Signaling ◽  
Glycogen Synthase ◽  
Insulin Metabolism ◽  
Relative Significance ◽  
Differentiated Cells ◽  
Mature Neuron ◽  
The Right ◽  
The Impact

AbstractRecently neuronal insulin resistance was suggested playing a role in Alzheimer’s disease. Streptozotocin (STZ) is commonly used to induce impairment in insulin metabolism. In our previous work on undifferentiated SH-SY5Y cells the compound exerted cytotoxicity without altering insulin sensitivity. Nevertheless, differentiation of the cells to a more mature neuron-like phenotype may considerably affect the significance of insulin signaling and its sensitivity to STZ. We aimed at studying the influence of STZ treatment on insulin signaling in SH-SY5Y cells differentiated by retinoic acid (RA). Cytotoxicity of STZ or low serum (LS) condition and protective effect of insulin were compared in RA differentiated SH-SY5Y cells. The effect of insulin and an incretin analogue, exendin-4 on insulin signaling was also examined by assessing glycogen synthase kinase-3 (GSK-3) phosphorylation. STZ was found less cytotoxic in the differentiated cells compared to our previous results in undifferentiated SH-SY5Y cells. The cytoprotective concentration of insulin was similar in the STZ and LS groups. However, the right-shifted concentration–response curve of insulin induced GSK-3 phosphorylation in STZ-treated differentiated cells is suggestive of the development of insulin resistance that was further confirmed by the insulin potentiating effect of exendin-4. Differentiation reduced the sensitivity of SH-SY5Y cells for the non-specific cytotoxicity of STZ and enhanced the relative significance of development of insulin resistance. The differentiated cells thus serve as a better model for studying the role of insulin signaling in neuronal survival. However, direct cytotoxicity of STZ also contributes to the cell death.

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