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Journal articles on the topic 'Glomus cell'

Author: Grafiati

Published: 4 June 2021

Last updated: 5 February 2022

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Neufeld, Meir, Jacob Pe'er, Eliezer Rosenman, and Moshe Lazar. "Intraorbital Glomus Cell Tumor." American Journal of Ophthalmology 117, no. 4 (1994): 539–41. http://dx.doi.org/10.1016/s0002-9394(14)70022-4.

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M, Neufeld, Pe??er J, Rosenman E, and Lazar M. "Intraorbital Glomus Cell Tumor." Journal of Neuro-Ophthalmology 14, no. 4 (1994): 222. http://dx.doi.org/10.1097/00041327-199412000-00037.

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Boyacioglu, Hatice, Nagihan Koc, Nihal Avcu, and Ozay Gokoz. "Glomus Tumour of the Lip Mimicking Squamous Cell Carcinoma - A Rare Case Report." Journal of Evolution of Medical and Dental Sciences 10, no. 9 (2021): 649–51. http://dx.doi.org/10.14260/jemds/2021/138.

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Glomus tumour is a rare soft tissue neoplasm arising from glomus body, which is in an arteriovenous anastomosis located particularly in the dermis. This tumour occurs most commonly in hands and feet, and is seldom found in other sites. The purpose of this report is to describe an unusual case of glomus tumour in the lip. A 17-year-old woman with a firm, painless and ulcerated lump in her lower lip was admitted to our clinic. Excisional biopsy was performed, and histopathological analysis revealed the lesion to be a subtype of glomus tumour called as a glomangioma. Most glomus tumours are benign and may be treated by simple surgical excision. A typical glomus tumour of the hand is readily diagnosed, but it may occur anywhere such as oral cavity or internal organs, and its small size and atypical anatomical site presents a diagnostic dilemma. Therefore, a glomus tumour should be considered in the differential diagnosis of mass in the lips. Glomus tumour was first mentioned by Wood as a painful subcutaneous tubercle.1,2 It is classified as a pericystic (perivascular) tumour by the World Health Organization. Perivascular tumours are most frequently noticed in the superficial soft tissues at any age and are not seen commonly in the oral cavity. Synonyms for glomus tumour include glomangioma, glomangiomyoma, glomangiomatosis, glomangiopericytoma, and Popoff tumour. 3 Glomus tumour is presumed to arise from glomus body, which may be defined as a special arteriovenous anastomosis located in the stratum reticular of the dermis. It is lined by smooth muscle and glomus cells.4 The glomus body has been implicated in playing a role in thermal regulation.5 It is ubiquitous but digits are the most common sites. Clinically, the lesion is usually seen as a painful nodule located in the nail bed of the distal phalanges. Occurrence in the oral cavity is particularly rare. In this article, we present a rare case of glomus tumour located in the lower lip mimicking a malignant tumour.

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Roy, Arijit, Jinqing Li, Abu-Bakr Al-Mehdi, Anil Mokashi та Sukhamay Lahiri. "Effect of acute hypoxia on glomus cell E mand ψm as measured by fluorescence imaging". Journal of Applied Physiology 93, № 6 (2002): 1987–98. http://dx.doi.org/10.1152/japplphysiol.00725.2001.

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We have reinvestigated the hypothesis of the relative importance of glomus cell plasma and mitochondrial membrane potentials ( E m and ψm, respectively) in acute hypoxia by a noninvasive fluorescence microimaging technique using the voltage-sensitive dyes bis-oxonol and JC-1, respectively. Short-term (24 h)-cultured rat glomus cells and cultured PC-12 cells were used for the study. Glomus cell E m depolarization was indirectly confirmed by an increase in bis-oxonol (an anionic probe) fluorescence due to a graded increase in extracellular K+. Fluorescence responses of glomus cell E m to acute hypoxia (∼10 Torr Po 2) indicated depolarization in 20%, no response in 45%, and hyperpolarization in 35% of the cells tested, whereas all PC-12 cells consistently depolarized in response to hypoxia. Furthermore, glomus cell E mhyperpolarization was confirmed with high CO (∼500 Torr). Glomus cell ψm depolarization was indirectly assessed by a decrease in JC-1 (a cationic probe) fluorescence. Accordingly, 1 μM carbonyl cyanide p-trifluoromethoxyphenylhydrazone (an uncoupler of oxidative phosphorylation), high CO (a metabolic inhibitor), and acute hypoxia (∼10 Torr Po 2) consistently depolarized the mitochondria in all glomus cells tested. Likewise, all PC-12 cell mitochondria depolarized in response to FCCP and hypoxia. Thus, although bis-oxonol could not show glomus cell depolarization consistently, JC-1 monitored glomus cell mitochondrial depolarization as an inevitable phenomenon in hypoxia. Overall, these responses supported our “metabomembrane hypothesis” of chemoreception.

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Saxe, Stephen J., Hans E. Grossniklaus, Ted H. Wojno, Gary L. Hertzler, Milton Boniuk, and Ramon L. Font. "Glomus Cell Tumor of the Eyelid." Ophthalmology 100, no. 1 (1993): 139–43. http://dx.doi.org/10.1016/s0161-6420(93)31710-0.

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Pribila, Jonathan T. "Glomus Cell Tumor of the Orbit." Archives of Ophthalmology 128, no. 1 (2010): 144. http://dx.doi.org/10.1001/archophthalmol.2009.359.

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Zhou, Ting, Ming-Shan Chien, Safa Kaleem, and Hiroaki Matsunami. "Single cell transcriptome analysis of mouse carotid body glomus cells." Journal of Physiology 594, no. 15 (2016): 4225–51. http://dx.doi.org/10.1113/jp271936.

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Liao, Zhiwei, Chao Chen, Bingjin Wang, and Cao Yang. "Minimally invasive resection of a glomus tumor of the thoracic spine: a case report and literature review." Journal of International Medical Research 47, no. 6 (2019): 2746–53. http://dx.doi.org/10.1177/0300060519847340.

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Objective Spinal involvement of glomus tumors is extremely rare. We herein present a case of a spinal glomus tumor and reviewed the literature to identify the most effective surgical treatment of spinal glomus tumors. Methods A 48-year-old man presented with a huge paravertebral space-occupying lesion. In this report, we present the diagnostic process and surgical procedure in this case and review the literature of glomus tumors with spine involvement. Results We suspected a primary diagnosis of neurilemmoma based on the imaging results; however, the postoperative pathologic examination confirmed a glomus tumor. Considering the size of the tumor and involvement of surrounding areas, we performed complete tumor resection and unilateral fusion with pedicle screws at the T2 to T4 level. This unilateral approach with fixation was less invasive than the standard open posterior approaches that are used when one side of the spinal canal is intact without bony destruction. Conclusions Surgical resection is a suitable treatment for most symptomatic glomus tumors. For most glomus tumors with spine involvement, total tumor resection with suitable internal fixation and fusion is recommended.

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PHILIPOV, Stanislav, Ivan MASLARSKI, Mariya KOLEVA-IVANOVA, and Dorian DIKOV. "Glomus coccygeum in pilonidal sinus surgical specimens: report of two rare cases with special reference to SOX10 expression." Anatomy 14, no. 3 (2020): 216–19. http://dx.doi.org/10.2399/ana.20.792465.

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We report two new cases of glomus coccygeum in pilonidal sinus excision specimens. The positive expression of glomus coccygeum cells for SOX10 is used for the first time. SOX10 is a useful immunohistochemical marker for identifying this microanatomical structure, confirming the diagnosis and may help the differential diagnosis. The glomus coccygeum cells are probably neural crest-derived from multipotent Schwann cell precursors.

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Li, Yu-Long, Hong Zheng, Yanfeng Ding, and Harold D. Schultz. "Expression of Neuronal Nitric Oxide Synthase in Rabbit Carotid Body Glomus Cells Regulates Large-Conductance Ca2+-Activated Potassium Currents." Journal of Neurophysiology 103, no. 6 (2010): 3027–33. http://dx.doi.org/10.1152/jn.01138.2009.

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Our previous studies show that a decrease in endogenous nitric oxide (NO) is involved in the blunted outward K+ currents in carotid body (CB) glomus cells from chronic heart failure (CHF) rabbits. In the present study, we measured the effects of the neuronal nitric oxide synthase (nNOS) transgene on the K+ currents in CB glomus cells from pacing-induced CHF rabbits. Using single-cell real-time RT-PCR and immunofluorescent techniques, we found that nNOS mRNA and protein are expressed in the rabbit CB glomus cells and CHF decreased the expression of nNOS mRNA and protein in CB glomus cells. After 3 days of an adenoviral nNOS (Ad.nNOS) gene transfection, the expression of nNOS protein was increased to the level found in sham CB glomus cells. In whole cell patch-clamp experiments, Ad.nNOS markedly reversed the attenuated K+ currents in CB glomus cells from CHF rabbits. The specific nNOS inhibitor (S-methyl-l-thiocitrulline [SMTC]) and large-conductance Ca2+-activated K+ (BK) channel blocker (iberiotoxin) fully abolished the effect of Ad.nNOS on the K+ currents in the CB glomus cells from CHF rabbits. However, neither CHF nor Ad.nNOS altered the protein expression of BK channel α-subunit. These results suggest that a decrease of NO induced by an attenuated nNOS activity lowers the activation of the BK channels but not the protein expression of the BK channel α-subunit in the CB glomus cells during CHF.

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Boileau, M. A., J. C. Grotta, A. Borit, et al. "Metastatic Renal Cell Carcinoma Simulating Glomus Jugulare Tumor." Journal of Urology 139, no. 4 (1988): 877. http://dx.doi.org/10.1016/s0022-5347(17)42669-3.

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Ekambar Eshwara Reddy, C., Naresh K. Panda, Gilbert Pragachi, Kusum Joshi, and J. Rajiv Bapuraj. "Petro-occipital Giant Cell Tumour Mimicking Glomus Jugulare." Journal of Otolaryngology 34, no. 05 (2005): 359. http://dx.doi.org/10.2310/7070.2005.34512.

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Eyzaguirre, C., Y. Hayashida, and L. Monti-Bloch. "Effects of denervation on the glomus cell membrane." Brain Research 524, no. 1 (1990): 164–70. http://dx.doi.org/10.1016/0006-8993(90)90508-9.

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Overholt, Jeffrey L., and Nanduri R. Prabhakar. "Ca2+ Current in Rabbit Carotid Body Glomus Cells Is Conducted by Multiple Types of High-Voltage–Activated Ca2+ Channels." Journal of Neurophysiology 78, no. 5 (1997): 2467–74. http://dx.doi.org/10.1152/jn.1997.78.5.2467.

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Overholt, Jeffrey L. and Nanduri R. Prabhakar. Ca2+ current in rabbit carotid body glomus cells is conducted by multiple types of high-voltage–activated Ca2+ channels. J. Neurophysiol. 78: 2467–2474, 1997. Carotid bodies are sensory organs that detect changes in arterial oxygen. Glomus cells are presumed to be the initial sites for sensory transduction, and Ca2+-dependent neurotransmitter release from glomus cells is believed to be an obligatory step in this response. Some information exists on the Ca2+ channels in rat glomus cells. However, relatively little is known about the types of Ca2+ channels present in rabbit glomus cells, the species in which most of the neurotransmitter release studies have been performed. Therefore we tested the effect of specific Ca2+ channel blockers on current recorded from freshly dissociated, adult rabbit carotid body glomus cells using the whole cell configuration of the patch-clamp technique. Macroscopic Ba2+ current elicited from a holding potential of −80 mV activated at a V m of approximaely −30 mV, peaked between 0 and +10 mV and did not inactivate during 25-ms steps to positive test potentials. Prolonged (≈2 min) depolarized holding potentials inactivated the current with a V 1/2 of −47 mV. There was no evidence for T-type channels. On steps to 0 mV, 6 mM Co2+ decreased peak inward current by 97 ± 1% (mean ± SE). Nisoldipine (2 μM), 1 μM ω-conotoxin GVIA, and 100 nM ω-agatoxin IVa each blocked a portion of the macroscopic Ca2+ current (30 ± 5, 33 ± 5, and 19 ± 3% after rundown correction, respectively). Simultaneous application of these blockers revealed a resistant current that was not affected by 1 μMω-conotoxin MVIIC. This resistant current constituted 27 ± 5% of the total macroscopic Ca2+ current. Each blocker had an effect in every cell so tested. However, the relative proportion of current blocked varied from cell to cell. These results suggest that L, N, P, and resistant channel types each conduct a significant proportion of the macroscopic Ca2+ current in rabbit glomus cells. Hypoxia-induced neurotransmitter release from glomus cells may involve one or more of these channels.

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Dagur, Gautam, Kelly Warren, Yimei Miao, Navjot Singh, Yiji Suh, and Sardar A. Khan. "Unusual Glomus Tumor of the Penis." Current Urology 9, no. 3 (2015): 113–18. http://dx.doi.org/10.1159/000442864.

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Introduction: Glomus tumors are benign neoplasms commonly found in subungual regions of the extremities and rarely located in the penis. Misdiagnosis of glomus tumors is common; therefore, symptoms and clinical presentations should be reviewed. Objective: The primary objective of this review article is to emphasize the pathogenesis, pathology, clinical presentation, symptoms, diagnosis, and treatment methods of glomus tumors in order to better identify and manage the condition. Materials and Methods: Research was conducted using PubMed/Medline. The inclusion criteria required glomus tumor to be present on the penis. Results: Glomus tumors, which appear as symptomatic or asymptomatic lesions, are attributed to dispersion grouping of neoplastic or non-neoplastic lesions in a particular area. Conclusion: Differential diagnosis of glomus tumors includes hemangiomas, neurofibromatosis, epithelial lesions, and spindle-cell lesions. Physical examination and histological findings should be used for diagnosis. Treatment options can be either conservative or invasive, in which the patient undergoes surgical excision.

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Cheng, P. M., and D. F. Donnelly. "Relationship between changes of glomus cell current and neural response of rat carotid body." Journal of Neurophysiology 74, no. 5 (1995): 2077–86. http://dx.doi.org/10.1152/jn.1995.74.5.2077.

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1. Mature rat carotid bodies were harvested and sinus nerve activity was recorded in vitro during superfusion with Ringer saline. Membrane currents of glomus cells were simultaneously recorded using conventional whole cell or perforated-patch whole cell recording. Presumptive glomus cells were identified by the presence of a rapidly activated, voltage-dependent outward current above a threshold of -20 mV. 2. Outward current of presumptive glomus cells was inhibited by tetraethylammonium chloride (TEA) (20 mM) and by verapamil (5-10 microM), consistent with previous studies in which isolated glomus cells were used. Somal capacitance, calculated from the current transient following a step hyperpolarization, was 7.47 +/- 0.54 (SE) pF (n = 52). Membrane resistance for perforated-patch recordings was 820 +/- 187 M omega. 3. In perforated-patch recordings, brief periods of hypoxia (30-45 s) caused a marked increase in nerve activity to 21.6 +/- 2.7 times baseline spiking frequency (n = 59) but no significant change in membrane resistance or outward current. No change in holding current was detected, although the low amplifier gain precluded high-resolution measurement. Similar results were obtained using conventional whole cell recording, except that outward current significantly decreased during hypoxia but failed to recover in the immediate posthypoxia period. 4. TEA (20 mM) rapidly inhibited outward current to 55 +/- 7% (n = 15) of predrug current, but nerve activity only slightly increased to 2.0 +/- 0.3 times baseline spike frequency (n = 15). Brief anoxia (40 s in duration) in the presence of TEA evoked a brisk increase in nerve activity to 30 +/- 13 times baseline frequency (n = 3), demonstrating that organ function was not blocked by TEA. 5. Charybdotoxin (10 nM) significantly reduced outward current by 12.1 +/- 3.0% (n = 11) but did not significantly alter nerve activity, holding current, or membrane resistance. Apamin (100 nM) did not significantly affect nerve activity, membrane resistance, or holding current. Outward current decreased by 11.4 +/- 6.1% (n = 13). 6. These results show a dissociation between changes in glomus cell voltage-gated outward currents and changes in afferent nerve activity. This suggests that modulation of glomus cell K+ current by hypoxia is not the primary step in initiating the nerve response to hypoxia in the rat carotid body.

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Graadt van Roggen, Joekes, Welvaart, and M van Krieken. "Unusual presentation of multiple subcutaneous glomus tumours of the lower limb with extensive glomus cell hyperplasia." Histopathology 34, no. 5 (1999): 474–75. http://dx.doi.org/10.1046/j.1365-2559.1999.0676c.x.

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Stea, A., and C. A. Nurse. "Chloride channels in cultured glomus cells of the rat carotid body." American Journal of Physiology-Cell Physiology 257, no. 2 (1989): C174—C181. http://dx.doi.org/10.1152/ajpcell.1989.257.2.c174.

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As part of our investigations on the chemosensory mechanisms in the rat carotid body, we are studying the physiology of the parenchymal glomus cells by the patch-clamp technique. Here we characterize a large-conductance chloride channel (approximately 296 pS) with random open and closed kinetics in inside-out patches of cultured glomus cells. The open-state probability (Po; mean = 0.61) was hardly affected by membrane potential (-50 to +50 mV) and cytoplasmic calcium (0-1 mM). Similarly, the channel did not appear to be regulated by cytoplasmic nucleotides (1 mM) or pH (6.5-8). Ion-substitution experiments yielded the following selectivity sequence: chloride greater than bicarbonate greater than sulfate greater than glutamate approximately sodium. Single-channel currents were reversibly reduced or blocked by anthracene-9-carboxylic acid (5-10 mM) but were unaffected by stilbene derivatives (0.5-1 mM), by furosemide (1 mM), and by 5-nitro-2-(3-phenyl-propylamino)benzoic acid (0.01 mM). Because these cultured glomus cells have been shown to express carbonic anhydrase, it is inferred that the chloride channels may play an important role in the physiology of glomus cells by aiding in the regulation of pHi and the resting potential via bicarbonate and chloride permeability.

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Bishop, Tammie, та Peter J. Ratcliffe. "Genetic basis of oxygen sensing in the carotid body: HIF2α and an isoform switch in cytochrome c oxidase subunit 4". Science Signaling 13, № 615 (2020): eaba1302. http://dx.doi.org/10.1126/scisignal.aba1302.

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The mechanistic basis of the marked oxygen sensitivity of glomus cells in the carotid body has long puzzled physiologists. In this issue of Science Signaling, Moreno-Domínguez et al. show the critical importance of high levels of hypoxia-inducible factor, HIF2α/EPAS1, and the nuclear-encoded mitochondrial cytochrome c oxidase subunit, COX4I2, in glomus cell sensitivity to hypoxia.

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Błaszkowski, Janusz, Tadeusz Madej, and Mariusz Tadych. "Glomus rubiforme, an arbuscular mycorrhizal fungus new to the mycota of Poland." Acta Mycologica 33, no. 2 (2014): 255–63. http://dx.doi.org/10.5586/am.1998.021.

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Glomus rubiforme is described and illustrated. as well as its occurrence in Poland and in the world is presented. Glomus rubiforme forms pale yellow to light brown spores arranged in blackberry-like sporocarps. The spores develop from a centrally positioned, inflated, thick-walled cell. The spore wall consists of two layers: a sloughing, hyaline outer layer adherent to a coloured, laminated layer. Glomus rubiforme is a new arbuscular mycorrhizal fungus to the mycota of Poland.

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Hempleman, S. C. "Increased calcium current in carotid body glomus cells following in vivo acclimatization to chronic hypoxia." Journal of Neurophysiology 76, no. 3 (1996): 1880–86. http://dx.doi.org/10.1152/jn.1996.76.3.1880.

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1. Rat pups were gestated and born in normoxia (inspired O2 pressure 149 mmHg) or chronic hypoxia (insured O2 pressure 80 mmHg) to test whether chronic hypoxia alters carotid body glomus cell calcium currents. Carotid bodies were removed from 5- to 8-day-old-pups under halothane anesthesia, at which time blood hematocrits averaged 52 +/- 1% (mean +/- SE) in the chronically hypoxic pups and 36 +/- 1% in the normoxic pups (P < 0.05). Glomus cells were then enzymatically isolated from the carotid bodies, and calcium currents were recorded with whole cell patch clamp. 2. Compared with normoxic glomus cells (n = 29), chronically hypoxic glomus cells (n = 32) superfused with 10 mM CaCl2 had larger peak calcium current (146 +/- 16 pA vs. 49 +/- 7 pA, P < 0.05), larger peak calcium current density (12.0 +/- 1.1 pA/pF vs. 7.3 +/- 1.0 pA/pF, P < 0.05), and larger membrane capacitance (12.1 +/- 0.9 pF vs. 7.5 +/- 0.6 pF, P < 0.05). 3. Threshold for calcium current activation was approximately -40 mV. Currents showed little inactivation during 45-ms test pulses and were half-inactivated by a steady holding voltage of -11 +/- 2 mV (n = 15). Currents were reduced 43 +/- 13% by 50 microM nifedipine (n = 6, P < 0.05), and were augmented with barium as the charge carrier. These properties suggest that glomus cell calcium current is carried in part through L-type channels, and that is is relatively resistant to steady-state inactivation. 4. Augmented calcium influx through voltage-gated channels in glomus cells from chronically hypoxic neonatal rats may increase carotid body excitability through increased stimulus-secretion coupling. Overall, acclimatization to chronic hypoxia is known to depress acute hypoxic ventilatory reflex responses in neonates. The observations reported here suggest that inhibition of ventilatory reflexes by chronic hypoxia in neonates occurs centrally rather than peripherally.

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Ortega-Sáenz, Patricia, Konstantin L. Levitsky, María T. Marcos-Almaraz, Victoria Bonilla-Henao, Alberto Pascual, and José López-Barneo. "Carotid body chemosensory responses in mice deficient of TASK channels." Journal of General Physiology 135, no. 4 (2010): 379–92. http://dx.doi.org/10.1085/jgp.200910302.

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Background K+ channels of the TASK family are believed to participate in sensory transduction by chemoreceptor (glomus) cells of the carotid body (CB). However, studies on the systemic CB-mediated ventilatory response to hypoxia and hypercapnia in TASK1- and/or TASK3-deficient mice have yielded conflicting results. We have characterized the glomus cell phenotype of TASK-null mice and studied the responses of individual cells to hypoxia and other chemical stimuli. CB morphology and glomus cell size were normal in wild-type as well as in TASK1−/− or double TASK1/3−/− mice. Patch-clamped TASK1/3-null glomus cells had significantly higher membrane resistance and less hyperpolarized resting potential than their wild-type counterpart. These electrical parameters were practically normal in TASK1−/− cells. Sensitivity of background currents to changes of extracellular pH was drastically diminished in TASK1/3-null cells. In contrast with these observations, responsiveness to hypoxia or hypercapnia of either TASK1−/− or double TASK1/3−/− cells, as estimated by the amperometric measurement of catecholamine release, was apparently normal. TASK1/3 knockout cells showed an enhanced secretory rate in basal (normoxic) conditions compatible with their increased excitability. Responsiveness to hypoxia of TASK1/3-null cells was maintained after pharmacological blockade of maxi-K+ channels. These data in the TASK-null mouse model indicate that TASK3 channels contribute to the background K+ current in glomus cells and to their sensitivity to external pH. They also suggest that, although TASK1 channels might be dispensable for O2/CO2 sensing in mouse CB cells, TASK3 channels (or TASK1/3 heteromers) could mediate hypoxic depolarization of normal glomus cells. The ability of TASK1/3−/− glomus cells to maintain a powerful response to hypoxia even after blockade of maxi-K+ channels, suggests the existence of multiple sensor and/or effector mechanisms, which could confer upon the cells a high adaptability to maintain their chemosensory function.

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Overholt, Jeffrey L., Eckhard Ficker, Tianen Yang, Hashim Shams, Gary R. Bright, and Nanduri R. Prabhakar. "HERG-Like Potassium Current Regulates the Resting Membrane Potential in Glomus Cells of the Rabbit Carotid Body." Journal of Neurophysiology 83, no. 3 (2000): 1150–57. http://dx.doi.org/10.1152/jn.2000.83.3.1150.

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Direct evidence for a specific K+ channel underlying the resting membrane potential in glomus cells of the carotid body has been absent. The product of the human ether-a-go-go–related gene (HERG) produces inward rectifier currents that are known to contribute to the resting membrane potential in other neuronal cells. The goal of the present study was to determine whether carotid body glomus cells express HERG-like K+ current, and if so, to determine whether a HERG-like current regulates the resting membrane potential. Freshly dissociated rabbit glomus cells under whole cell voltage clamp exhibited slowly decaying outward currents that activated 20–30 mV positive to the resting membrane potential. Raising extracellular K+revealed a slowly deactivating inward tail current indicative of HERG-like K+ current. HERG-like currents were not found in cells resembling type II cells. The HERG-like current was blocked by dofetilide (DOF) in a concentration-dependent manner (IC50 = 13 ± 4 nM, mean ± SE) and high concentrations of Ba2+ (1 and 10 mM). The biophysical and pharmacological characteristics of this inward tail current suggest that it is conducted by a HERG-like channel. The steady-state activation properties of the HERG-like current ( V h = −44 ± 2 mV) suggest that it is active at the resting membrane potential in glomus cells. In whole cell, current-clamped glomus cells (average resting membrane potential, − 48 ± 4 mV), DOF, but not tetraethylammonium, caused a significant (13 mV) depolarizing shift in the resting membrane potential. Using fluorescence imaging, DOF increased [Ca2+]i in isolated glomus cells. In an in-vitro carotid body preparation, DOF increased basal sensory discharge in the carotid sinus nerve in a concentration-dependent manner. These results demonstrate that glomus cells express a HERG-like current that is active at, and responsible for controlling the resting membrane potential.

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Conte, Alessandro, Emma Scurrell, and Stephen J. Baines. "Glomus cell tumour on the head of a cat." Journal of Feline Medicine and Surgery Open Reports 4, no. 2 (2018): 205511691880103. http://dx.doi.org/10.1177/2055116918801033.

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Case summary A solitary, sessile, non-ulcerated, freely mobile cutaneous mass approximately 1 cm in diameter on the left temporal region of a 7-year-old neutered female cat was examined. A fine-needle aspirate and wedge biopsy were performed by the referring veterinary surgeon and indicated a neoplasm of uncertain cell lineage. On histopathological examination, the deep dermis contained a discrete, non-encapsulated and vascular neoplasm with morphological and immunophenotypical features typical of a glomus cell tumour. Neoplastic cells were immunopositive for vimentin, muscle actin and smooth muscle actin, and immunonegative for cytokeratin, S100, desmin and von Willebrand factor (factor VIII-related antigen). Relevance and novel information Glomus cell tumours arise from modified smooth muscle cells and are rare in animals, particularly cats. Specific immunohistochemistry is of fundamental importance in the correct diagnosis of these tumours and should be considered for masses when cytology and histology results are inconclusive or uncertain.

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Koske, R. E. "Glomus aggregatum Emended: A Distinct Taxon in the Glomus fasciculatum Complex." Mycologia 77, no. 4 (1985): 619. http://dx.doi.org/10.2307/3793360.

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Koske, R. E. "Glomus Aggregatum Emended: A Distinct Taxon in the Glomus Fasciculatum Complex." Mycologia 77, no. 4 (1985): 619–30. http://dx.doi.org/10.1080/00275514.1985.12025147.

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KUSAKABE, Tatsumi. "The occurrence of melanosomes in the newt glomus cell." Archives of Histology and Cytology 54, no. 1 (1991): 81–87. http://dx.doi.org/10.1679/aohc.54.81.

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Carroll, John L., and Insook Kim. "Postnatal development of carotid body glomus cell O2 sensitivity." Respiratory Physiology & Neurobiology 149, no. 1-3 (2005): 201–15. http://dx.doi.org/10.1016/j.resp.2005.04.009.

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LEVER, L. R., and P. J. A. HOLT. "Multiple glomus cell tumours-treatment by infra-red coagulation." Clinical and Experimental Dermatology 17, no. 1 (1992): 34–35. http://dx.doi.org/10.1111/j.1365-2230.1992.tb02530.x.

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Hockman, Dorit, Igor Adameyko, Marketa Kaucka, et al. "Striking parallels between carotid body glomus cell and adrenal chromaffin cell development." Developmental Biology 444 (December 2018): S308—S324. http://dx.doi.org/10.1016/j.ydbio.2018.05.016.

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Sobrino, Verónica, Aida Platero-Luengo, Valentina Annese, et al. "Neurotransmitter Modulation of Carotid Body Germinal Niche." International Journal of Molecular Sciences 21, no. 21 (2020): 8231. http://dx.doi.org/10.3390/ijms21218231.

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The carotid body (CB), a neural-crest-derived organ and the main arterial chemoreceptor in mammals, is composed of clusters of cells called glomeruli. Each glomerulus contains neuron-like, O2-sensing glomus cells, which are innervated by sensory fibers of the petrosal ganglion and are located in close contact with a dense network of fenestrated capillaries. In response to hypoxia, glomus cells release transmitters to activate afferent fibers impinging on the respiratory and autonomic centers to induce hyperventilation and sympathetic activation. Glomus cells are embraced by interdigitating processes of sustentacular, glia-like, type II cells. The CB has an extraordinary structural plasticity, unusual for a neural tissue, as it can grow several folds its size in subjects exposed to sustained hypoxia (as for example in high altitude dwellers or in patients with cardiopulmonary diseases). CB growth in hypoxia is mainly due to the generation of new glomeruli and blood vessels. In recent years it has been shown that the adult CB contains a collection of quiescent multipotent stem cells, as well as immature progenitors committed to the neurogenic or the angiogenic lineages. Herein, we review the main properties of the different cell types in the CB germinal niche. We also summarize experimental data suggesting that O2-sensitive glomus cells are the master regulators of CB plasticity. Upon exposure to hypoxia, neurotransmitters and neuromodulators released by glomus cells act as paracrine signals that induce proliferation and differentiation of multipotent stem cells and progenitors, thus causing CB hypertrophy and an increased sensory output. Pharmacological modulation of glomus cell activity might constitute a useful clinical tool to fight pathologies associated with exaggerated sympathetic outflow due to CB overactivation.

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Mokashi, A., D. Ray, F. Botre, M. Katayama, S. Osanai, and S. Lahiri. "Effect of hypoxia on intracellular pH of glomus cells cultured from cat and rat carotid bodies." Journal of Applied Physiology 78, no. 5 (1995): 1875–81. http://dx.doi.org/10.1152/jappl.1995.78.5.1875.

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To test the hypothesis that hypoxia may induce cellular acidification during chemotransduction in the carotid body, we compared the effects of hypoxia and of extracellular acidosis on intracellular pH (pHi) of glomus cells cultured from rat and cat carotid bodies. The cells were prepared and cultured for 2–7 days. The plated cells were loaded with a pH-sensitive fluorescent probe, SNARF-1-acetoxymethyl ester, and were placed in a closed chamber and superfused. The effects of lowering PO2 and pH in the superfusion medium containing CO2-HCO3- buffer on the glomus cell pHi were measured at 37 degrees C. The pHi was measured in a single or a few isolated cells with single excitation at 540 nm and dual emission at 590 and 640 nm, after the exposure to different PO2 levels from 132 to 43, 14, and 1–2 Torr for 10–12 min in the closed chamber. The resting pHi values were 7.263 +/- 0.008 for rat and 7.175 +/- 0.004 for cat carotid body glomus cells. For a decrease of PO2 from 132 Torr to 14 Torr, the change in pHi values, on average, for cat and rat glomus cells was 0.034 lower, and with PO2 decrease to 1–2 Torr for the cat glomus cells, the change in pHi values was 0.051 lower. On the other hand, when the perfusate pH values were decreased from 7.4 to 6.9 during normoxia, the reduction of change in pHi values were 0.327 for the rat and 0.397 for the cat. Thus glomus cell pHi change due to low PO2 exposure was not significant and was not commensurate with the large increases in the chemosensory activity.

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Wang, Nan, Andy K. Lee, Lei Yan, Michael R. Simpson, Amy Tse, and Frederick W. Tse. "Granule matrix property and rapid “kiss-and-run” exocytosis contribute to the different kinetics of catecholamine release from carotid glomus and adrenal chromaffin cells at matched quantal size." Canadian Journal of Physiology and Pharmacology 90, no. 6 (2012): 791–801. http://dx.doi.org/10.1139/y2012-040.

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Catecholamine-containing small dense core granules (SDCGs, vesicular diameter of ∼100 nm) are prominent in carotid glomus (chemosensory) cells and some neurons, but the release kinetics from individual SDCGs has not been studied in detail. In this study, we compared the amperometric signals from glomus cells with those from adrenal chromaffin cells, which also secrete catecholamine but via large dense core granules (LDCGs, vesicular diameter of ∼200–250 nm). When exocytosis was triggered by whole-cell dialysis (which raised the concentration of intracellular Ca2+ ([Ca2+]i) to ∼0.5 µmol/L), the proportion of the type of signal that represents a flickering fusion pore was 9-fold higher for glomus cells. Yet, at the same range of quantal size (Q, the total amount of catecholamine that can be released from a granule), the kinetics of every phase of the amperometric spike signals from glomus cells was faster. Our data indicate that the last phenomenon involved at least 2 mechanisms: (i) the granule matrix of glomus cells can supply a higher concentration of free catecholamine during exocytosis; (ii) a modest elevation of [Ca2+]i triggers a form of rapid “kiss-and-run” exocytosis, which is very prevalent among glomus SDCGs and leads to incomplete release of their catecholamine content (and underestimation of their Q value).

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Sterni, L. M., O. S. Bamford, S. M. Tomares, M. H. Montrose, and J. L. Carroll. "Developmental changes in intracellular Ca2+ response of carotid chemoreceptor cells to hypoxia." American Journal of Physiology-Lung Cellular and Molecular Physiology 268, no. 5 (1995): L801—L808. http://dx.doi.org/10.1152/ajplung.1995.268.5.l801.

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The carotid chemoreceptor response to hypoxia is weak just after birth and increases during postnatal development. The mechanisms underlying chemoreceptor maturation are unknown. We tested the hypothesis that carotid chemoreceptor maturation occurs at the glomus cell level by measuring intracellular calcium ([Ca2+]i) mobilization in response to hypoxia, anoxia, and NaCN in freshly dissociated cells from newborn vs. adult rabbit carotid bodies. Cells were loaded with fura 2 and superfused at 37 degrees C with balanced salt solution equilibrated with 5% CO2. [Ca2+]i mobilization in response to 3-min challenges of hypoxia (PO2 approximately 15 mmHg), anoxia (PO2 approximately 0 mmHg), and NaCN (1 mM) was measured using a digital imaging microscope. The fluorescence intensity ratio was used to calculate [Ca2+]i. Peak [Ca2+]i responses to all three challenges were three- to fivefold greater in glomus cells from adult compared with newborn carotid chemoreceptors. In addition, the average normoxic [Ca2+]i baseline was approximately threefold higher in the adult glomus cells. These results suggest that carotid chemoreceptor glomus cell sensitivity to natural stimuli, as reflected by the [Ca2+]i response, depends on the level of postnatal maturity.

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Smith, George S., and N. C. Schenck. "Two New Dimorphic Species in the Endogonaceae: Glomus Ambisporum and Glomus Heterosporum." Mycologia 77, no. 4 (1985): 566–74. http://dx.doi.org/10.1080/00275514.1985.12025142.

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AL-QATTAN, M. M., and H. M. CLARKE. "An Isolated Granular Cell Tumour of the Thumb Pulp Clinically Mimicking a Glomus Tumour." Journal of Hand Surgery 19, no. 4 (1994): 420–21. http://dx.doi.org/10.1016/0266-7681(94)90201-1.

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A rare case of an isolated granular cell tumour of the thumb pulp clinically mimicking a glomus tumour is described. The rationale behind performing oestrogen receptor staining for granular cell tumours is discussed.

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Donnelly, David F. "Developmental aspects of oxygen sensing by the carotid body." Journal of Applied Physiology 88, no. 6 (2000): 2296–301. http://dx.doi.org/10.1152/jappl.2000.88.6.2296.

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The carotid body chemoreceptors, the major hypoxia sensory organs for the respiratory system, undergo a significant increase in their hypoxia responsiveness in the postnatal period. This is manifest by a higher level of afferent nerve activity for a given level of arterial oxygen tension. The mechanism for the enhanced sensitivity is unresolved, but most work has focused on the glomus cell, a secretory cell apposed to the afferent nerve ending and believed to be the site of hypoxia transduction. The glomus cell secretory response to hypoxia increases postnatally, and this is correlated with an enhanced calcium rise in response to hypoxia and an increase in oxygen-sensitive potassium currents. These changes are sensitive to the level of hypoxia in the postnatal period, and significant impairment of organ function is observed with postnatal hypoxia as well as postnatal hyperoxia. Although many questions remain, especially with regard to the coupling of glomus cells to nerve endings, the use of cellular and molecular techniques should offer resolution in the near future.

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Di Giulio, C., P. G. Data, and S. Lahiri. "Chronic cobalt causes hypertrophy of glomus cells in the rat carotid body." American Journal of Physiology-Cell Physiology 261, no. 1 (1991): C102—C105. http://dx.doi.org/10.1152/ajpcell.1991.261.1.c102.

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We tested the hypothesis that chronic cobalt administration would induce carotid body cellular response along with polycythemia as found in chronic hypoxia if common oxygen-sensitive mechanisms were involved in the two instances. Morphometric studies were performed on carotid bodies in male rats that were chronically treated with cobalt chloride (0.17 mumol/kg, ip, daily for 6 wk) and in control rats that received blank saline injections. The rats were anesthetized, blood samples were collected for hematocrit, and the carotid bodies were surgically exposed and were perfused and superfused with the buffered fixative (3% glutaraldehyde plus 1% paraformaldehyde, pH 7.40, 330-340 mosM). The carotid bodies were processed, and ultrathin sections were cut for electron microscopy and morphometry of type I (glomus) and type II cells. Hematocrit increased from 44% in the control to 74% in the cobalt-treated rats, and the mean volume of type I cells increased from 424 to 1,061 microns 3. Type II cells did not show any significant change in size. The results suggest that cobalt stimulated oxygen-sensitive mechanism in the glomus cells of the carotid body and that the glomus cell is a site of oxygen chemosensing.

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Schwaber, Mitchell K., Gerald S. Gussack, and Wanda Kirkpatrick. "The Role of Radiation Therapy in the Management of Catecholamine-Secreting Glomus Tumors." Otolaryngology–Head and Neck Surgery 98, no. 2 (1988): 150–54. http://dx.doi.org/10.1177/019459988809800209.

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The major source of controversy that surrounds the use of radiation for glomus tumors is the finding of persistent chief cells years after completion of the treatment. Questions have been raised as to the viability of the irradiated chief cell and its capacity to proliferate. The radiotherapists consider a stable glomus tumor a radiation “cure,” whereas skull base surgeons are fearful that these lesions will continue to slowly grow and cause problems 20 to 30 years later. We have recently managed a patient who was not a candidate for surgery, with a catecholamine-secreting glomus jugulare tumor. after 4750 rad of radiation therapy, no changes in tumor size or in catecholamine secretion have been observed (at 20 months of followup). The implications of the case are discussed.

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Wasicko, M. J., G. E. Breitwieser, I. Kim, and J. L. Carroll. "Postnatal development of carotid body glomus cell response to hypoxia." Respiratory Physiology & Neurobiology 154, no. 3 (2006): 356–71. http://dx.doi.org/10.1016/j.resp.2006.01.003.

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Sherpa, A. K., K. H. Albertine, D. G. Penney, B. Thompkins, and S. Lahiri. "Chronic CO exposure stimulates erythropoiesis but not glomus cell growth." Journal of Applied Physiology 67, no. 4 (1989): 1383–87. http://dx.doi.org/10.1152/jappl.1989.67.4.1383.

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The effect of chronic CO exposure, which stimulates erythropoietin production and erythropoiesis, was studied on carotid body cells in the rat. The hypothesis to be tested was that chronic CO inhalation would stimulate cellular hypertrophy and hyperplasia of carotid body if it caused local tissue hypoxia as in chronic hypoxia. The failure of an appropriate response would indicate a lack of a specific local effect on carotid body tissue PO2 presumably because of its unusually high tissue blood flow. Six young male rats were exposed to 0.4–0.5 Torr (0.05–0.07%) inspired PCO in air for 22 days. Control rats (n = 6) were maintained under similar conditions except for CO exposure. After the exposure period the rats were anesthetized, blood was collected for hematocrit, and the carotid bodies were surgically exposed and fixed for electron microscopy and morphometry of type I and type II cells and capillary endothelium. Hematocrit was significantly greater in the CO-exposed group (75 vs. 48%), whereas no significant difference was found in the carotid body parenchyma between the control and CO-exposed groups. We conclude that the lack of an effect of chronic CO exposure on the carotid bodies in contrast to the strong erythropoietic response indicates a relatively high tissue blood flow rate in the carotid body and that CO did not exert a direct cellular effect. The results also suggest that the hypertrophic response of carotid body glomus cells to chronic hypoxic hypoxia is the result of a local direct effect of low PO2 rather than secondary to systemic effects.

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Seo, Jeong Ho, Ho Seong Lee, Sang Woo Kim, Jae Jung Jeong, and Young Rak Choi. "Subungual Glomus Cell Proliferation in the Toe: A Case Report." Journal of Foot and Ankle Surgery 53, no. 5 (2014): 628–30. http://dx.doi.org/10.1053/j.jfas.2014.03.004.

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Pusztaszeri, Marc. "Glomus tumor of kidney: differential diagnosis from juxtaglomerular cell tumor." Human Pathology 43, no. 4 (2012): 616. http://dx.doi.org/10.1016/j.humpath.2011.12.009.

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Pandit, Jaideep J., Nicky Huskens, Peadar B. O’Donohoe, Philip J. Turner, and Keith J. Buckler. "Competitive Interactions between Halothane and Isoflurane at the Carotid Body and TASK Channels." Anesthesiology 133, no. 5 (2020): 1046–59. http://dx.doi.org/10.1097/aln.0000000000003520.

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Background The degree to which different volatile anesthetics depress carotid body hypoxic response relates to their ability to activate TASK potassium channels. Most commonly, volatile anesthetic pairs act additively at their molecular targets. We examined whether this applied to carotid body TASK channels. Methods We studied halothane and isoflurane effects on hypoxia-evoked rise in intracellular calcium (Ca2+i, using the indicator Indo-1) in isolated neonatal rat glomus cells, and TASK single-channel activity (patch clamping) in native glomus cells and HEK293 cell line cells transiently expressing TASK-1. Results Halothane (5%) depressed glomus cell Ca2+i hypoxic response (mean ± SD, 94 ± 4% depression; P &lt; 0.001 vs. control). Isoflurane (5%) had a less pronounced effect (53 ± 10% depression; P &lt; 0.001 vs. halothane). A mix of 3% isoflurane/1.5% halothane depressed cell Ca2+i response (51 ± 17% depression) to a lesser degree than 1.5% halothane alone (79 ± 15%; P = 0.001), but similar to 3% isoflurane alone (44 ± 22%; P = 0.224), indicating subadditivity. Halothane and isoflurane increased glomus cell TASK-1/TASK-3 activity, but mixes had a lesser effect than that seen with halothane alone: 4% halothane/4% isoflurane yielded channel open probabilities 127 ± 55% above control, versus 226 ± 12% for 4% halothane alone (P = 0.009). Finally, in HEK293 cell line cells, progressively adding isoflurane (1.5 to 5%) to halothane (2.5%) reduced TASK-1 channel activity from 120 ± 38% above control, to 88 ± 48% (P = 0.034). Conclusions In all three experimental models, the effects of isoflurane and halothane combinations were quantitatively consistent with the modeling of weak and strong agonists competing at a common receptor on the TASK channel. Editor’s Perspective What We Already Know about This Topic What This Article Tells Us That Is New

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Moreno-Domínguez, Alejandro, Patricia Ortega-Sáenz, Lin Gao та ін. "Acute O2 sensing through HIF2α-dependent expression of atypical cytochrome oxidase subunits in arterial chemoreceptors". Science Signaling 13, № 615 (2019): eaay9452. http://dx.doi.org/10.1126/scisignal.aay9452.

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Acute cardiorespiratory responses to O2 deficiency are essential for physiological homeostasis. The prototypical acute O2-sensing organ is the carotid body, which contains glomus cells expressing K+ channels whose inhibition by hypoxia leads to transmitter release and activation of nerve fibers terminating in the brainstem respiratory center. The mechanism by which changes in O2 tension modulate ion channels has remained elusive. Glomus cells express genes encoding HIF2α (Epas1) and atypical mitochondrial subunits at high levels, and mitochondrial NADH and reactive oxygen species (ROS) accumulation during hypoxia provides the signal that regulates ion channels. We report that inactivation of Epas1 in adult mice resulted in selective abolition of glomus cell responsiveness to acute hypoxia and the hypoxic ventilatory response. Epas1 deficiency led to the decreased expression of atypical mitochondrial subunits in the carotid body, and genetic deletion of Cox4i2 mimicked the defective hypoxic responses of Epas1-null mice. These findings provide a mechanistic explanation for the acute O2 regulation of breathing, reveal an unanticipated role of HIF2α, and link acute and chronic adaptive responses to hypoxia.

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Wilding, T. J., B. Cheng, and A. Roos. "pH regulation in adult rat carotid body glomus cells. Importance of extracellular pH, sodium, and potassium." Journal of General Physiology 100, no. 4 (1992): 593–608. http://dx.doi.org/10.1085/jgp.100.4.593.

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The course of intracellular pH (pHi) was followed in superfused (36 degrees C) single glomus (type I) cells of the freshly dissociated adult rat carotid body. The cells had been loaded with the pH-sensitive fluorescent dye 2',7'-(2-carboxyethyl)-5 (and -6)-carboxyfluorescein. The high K(+)-nigericin method was used for calibration. The pHi of the glomus cell at pHo 7.40, without CO2, was 7.23 +/- 0.02 (n = 70); in 5% CO2/25 mM HCO3-, pHi was 7.18 +/- 0.08 (n = 9). The pHi was very sensitive to changes in pHo. Without CO2, delta pHi/delta pHo was 0.85 (pHo 6.20-8.00; 32 cells), while in CO2/HCO3- this ratio was 0.82 irrespective of whether pHo (6.80-7.40; 14 cells) was changed at constant PCO2 or at constant [HCO3-]o. The great pHi sensitivity of the glomus cell to pHo is matched only by that of the human red cell. An active Na+/H+ exchanger (apparent Km = 58 +/- 6 mM) is present in glomus cells: Na+ removal or addition of the amiloride derivative 5-(N,N-hexamethylene)-amiloride induced pHi to fall by as much as 0.9. The membrane of these cells also contains a K+/H+ exchanger. Raising [K+]o from 4.7 to 25, 50, or 140 mM reversibly raised pHi by 0.2, 0.3, and 0.6, respectively. Rb+ had no effect, but in corresponding concentrations of Tl+ alkalinization was much faster than in K+. Reducing [K+]o to 1.5 mM lowered pHi by 0.1. These pHi changes were shown not to be due to changes in membrane voltage, and were even more striking in the absence of Na+. Intrinsic buffering power (amount of strong base required to produce, in the nominal absence of CO2, a small pHi rise) increased from 3 to approximately 21 mM as pHi was lowered, but remained nearly unchanged below pHi 6.60. The fitted expression assumed the presence of one "equivalent" intracellular buffer (pK 6.41, 41 mM). The exceptional pHi sensitivity to pHo suggests that the pHi of the glomus cell is a link in the chemoreceptor's response to external acidity.

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Wu, Chi-Guang, and David M. Sylvia. "Spore Ontogeny of Glomus globiferum." Mycologia 85, no. 2 (1993): 317. http://dx.doi.org/10.2307/3760465.

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Makarenko, Vladislav V., Gias U. Ahmmed, Ying-Jie Peng, et al. "CaV3.2 T-type Ca2+ channels mediate the augmented calcium influx in carotid body glomus cells by chronic intermittent hypoxia." Journal of Neurophysiology 115, no. 1 (2016): 345–54. http://dx.doi.org/10.1152/jn.00775.2015.

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Chronic intermittent hypoxia (CIH) is a hallmark manifestation of sleep apnea. A heightened carotid body activity and the resulting chemosensory reflex mediate increased sympathetic nerve activity by CIH. However, the mechanisms underlying heightened carotid body activity by CIH are not known. An elevation of intracellular calcium ion concentration ([Ca2+]i) in glomus cells, the primary oxygen-sensing cells, is an essential step for carotid body activation by hypoxia. In the present study, we examined the effects of CIH on the glomus cell [Ca2+]i response to hypoxia and assessed the underlying mechanisms. Glomus cells were harvested from adult rats or wild-type mice treated with 10 days of either room air (control) or CIH (alternating cycles of 15 s of hypoxia and 5 min of room air; 9 episodes/h; 8 h/day). CIH-treated glomus cells exhibited an enhanced [Ca2+]i response to hypoxia, and this effect was absent in the presence of 2-(4-cyclopropylphenyl)- N-((1R)-1-[5-[(2,2,2-trifluoroethyl)oxo]-pyridin-2-yl]ethyl)acetamide (TTA-A2), a specific inhibitor of T-type Ca2+ channels, and in voltage-gated calcium channel, type 3.2 (CaV3.2), null glomus cells. CaV3.2 knockout mice exhibited an absence of CIH-induced hypersensitivity of the carotid body. CIH increased reactive oxygen species (ROS) levels in glomus cells. A ROS scavenger prevented the exaggerated TTA-A2-sensitive [Ca2+]i response to hypoxia. CIH had no effect on CaV3.2 mRNA levels. CIH augmented Ca2+ currents and increased CaV3.2 protein in plasma membrane fractions of human embryonic kidney-293 cells stably expressing CaV3.2, and either a ROS scavenger or brefeldin-A, an inhibitor of protein trafficking, prevented these effects. These findings suggest that CIH leads to an augmented Ca2+ influx via ROS-dependent facilitation of CaV3.2 protein trafficking to the plasma membrane.

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Piruat, José I., C. Oscar Pintado, Patricia Ortega-Sáenz, Marta Roche, and José López-Barneo. "The Mitochondrial SDHD Gene Is Required for Early Embryogenesis, and Its Partial Deficiency Results in Persistent Carotid Body Glomus Cell Activation with Full Responsiveness to Hypoxia." Molecular and Cellular Biology 24, no. 24 (2004): 10933–40. http://dx.doi.org/10.1128/mcb.24.24.10933-10940.2004.

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ABSTRACT The SDHD gene encodes one of the two membrane-anchoring proteins of the succinate dehydrogenase (complex II) of the mitochondrial electron transport chain. This gene has recently been proposed to be involved in oxygen sensing because mutations that cause loss of its function produce hereditary familiar paraganglioma, a tumor of the carotid body (CB), the main arterial chemoreceptor that senses oxygen levels in the blood. Here, we report the generation of a SDHD knockout mouse, which to our knowledge is the first mammalian model lacking a protein of the electron transport chain. Homozygous SDHD −/− animals die at early embryonic stages. Heterozygous SDHD +/− mice show a general, noncompensated deficiency of succinate dehydrogenase activity without alterations in body weight or major physiological dysfunction. The responsiveness to hypoxia of CBs from SDHD +/− mice remains intact, although the loss of an SDHD allele results in abnormal enhancement of resting CB activity due to a decrease of K+ conductance and persistent Ca2+ influx into glomus cells. This CB overactivity is linked to a subtle glomus cell hypertrophy and hyperplasia. These observations indicate that constitutive activation of SDHD +/− glomus cells precedes CB tumor transformation. They also suggest that, contrary to previous beliefs, mitochondrial complex II is not directly involved in CB oxygen sensing.

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Chow, Louis Tsun Cheung, Michael Ho Ming Chan, and Simon Kwok Chuen Wong. "Functional Ulnar Nerve Paraganglioma: First Documented Occurrence in the Extremity With Hitherto Undescribed Associated Extensive Glomus Cell Hyperplasia and Tumorlet Formation." International Journal of Surgical Pathology 26, no. 1 (2017): 64–72. http://dx.doi.org/10.1177/1066896917720750.

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Extra-adrenal paraganglioma has never been described in the extremities. A 34-year-old woman complained of an enlarging mass in the right forearm for 18 months. Imaging showed a circumscribed vascular tumor attached to the ulnar nerve; biopsy revealed features of paraganglioma. The resected tumor consisted of zellballen pattern of chief cells staining positively for chromogranin with surrounding S100-positive sustentacular cells. The chief cells contained many neurosecretory granules and mitochondria, whereas the sustentacular cells contained a large amount of rough endoplasmic reticulum and some microfilaments. There was adjacent extensive glomus cell hyperplasia and tumorlet formation. The intraoperative blood pressure dropped abruptly on tumor removal. The serum normetanephrine level decreased from a preoperative level of 1987 pg/mL (normal < 149 pg/mL) to normal after operation. The patient admitted on questioning to a history of paroxysmal attacks of transient palpitation, hand tremors, and sweating; imaging showed no evidence of tumor in other parts of the body, and there was no family history of similar tumor; she remained well 33 months after the operation. This occurrence of functional ulnar nerve paraganglioma with the hitherto undescribed associated glomus cell hyperplasia and tumorlet formation attests to the probable existence of normal sympathetic paraganglia in the extremity and their intimate functional relationship with glomus bodies.

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