Abstract

The carotid body may undergo plasticity changes during development/ageing and in response to environmental (hypoxia and hyperoxia), metabolic, and inflammatory stimuli. The different cell types of the carotid body express a wide series of growth factors and corresponding receptors, which play a role in the modulation of carotid body function and plasticity. In particular, type I cells express nerve growth factor, brain-derived neurotrophic factor, neurotrophin 3, glial cell line-derived neurotrophic factor, ciliary neurotrophic factor, insulin-like-growth factor-I and -II, basic fibroblast growth factor, epidermal growth factor, transforming growth factor-α and -β, interleukin-1β and -6, tumor necrosis factor-α, vascular endothelial growth factor, and endothelin-1. Many specific growth factor receptors have been identified in type I cells, indicating autocrine/paracrine effects. Type II cells may also produce growth factors and express corresponding receptors. Future research will have to consider growth factors in further experimental models of cardiovascular, metabolic, and inflammatory diseases and in human (normal and pathologic) samples. From a methodological point of view, microarray and/or proteomic approaches would permit contemporary analyses of large groups of growth factors. The eventual identification of physical interactions between receptors of different growth factors and/or neuromodulators could also add insights regarding functional interactions between different trophic mechanisms.

Highlights

  • The carotid body (CB) is the main structure devoted to peripheral arterial chemoreception

  • The evaluation of chronic hyperoxia on postnatal CB development was the research target of Dmitrieff et al [25]; by mRNA expression studies and Western blot analysis, the authors demonstrated that a reduced signaling mediated by the TrkB receptors may have a role in CB hypoplasia

  • Nitric oxide synthase (NOS) immunoreactivity was higher in CB tissues from the children and young adult subjects compared with the old subjects, suggesting that oxygen-sensitive CB mechanisms are affected in an age-dependent manner [92]

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Summary

Introduction

The carotid body (CB) is the main structure devoted to peripheral arterial chemoreception. Type I cells produce many different neurotransmitters/neuromodulators and are considered the real chemoreceptive structures, whereas type II cells are usually considered supportive cells, enveloping type I cells. It has been stressed, that type II cells probably interact with type I cells for coordination of chemosensory transduction [4,5] and that type II cells are the stem cell precursors for type I cells [6]. According to the study results, a stronger NGF expression and a moderate NGF expression were detected in type I cells and in a subset of type II cells, respectively, in case of hypertension. The same expression pattern was observed for NGF receptors, TrkA, and p75 (Tables 1 and 2)

Brain-Derived Neurotrophic Factor
Detection Methods
Glial Cell Line-Derived Neurotrophic Factor Family of Ligands
Glial-Derived Neurotrophic Factor
Detection Methods In situ hybridization
Ciliary Neurotrophic Factor Family
Insulin and Insulin-Like Growth Factors
Detection Methods Double immunofluorescence Double immunofluorescence
Fibroblast Growth Factors
Transforming Growth Factor-β and Related Molecules
Inflammatory Cytokines
10. Vascular Endothelial Growth Factor
Detection Methods Immunohistochemistry Immunocytochemistry
11. Endothelins
12. Platelet-Derived Growth Factor
13. Receptor–Receptor Interactions involving Growth Factors Receptors
14. The Trophic Role of CB Grafting in Parkinson’s Disease
Findings
15. Conclusions
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