Umus, Astrid Pouwelsen and Jacqueline Kuhnen for the breeding of the

Umus, Astrid Pouwelsen and Jacqueline Kuhnen for the breeding of the mosquitoes and Anja Scholzen and Chris Janse for critical revision of the manuscript.Author ContributionsConceived and designed the experiments: IHJP HJC. Performed the experiments: IHJP HJC MWR. Analyzed the data: IHJP. Contributed reagents/materials/analysis tools: HJC GJvG CCH MWR. Wrote the paper: IHJP RWS.
Parafollicular cells or Thyroid C cells are FCCP site generally known for producing calcitonin, a hormone involved in calcium homeostasis with hypocalcemic and hypophosphatemic effects but it has been highlighted their role in the production of numerous regulatory peptides such as somatostatin and ghrelin [1], katacalcin I, katacalcin II, gastrin-releasing peptide, thyroliberin and helodermin [2]. Moreover C cells, under regulation by thyrotropin (TSH) because of TSH receptor (TSHR) expression, are involved in the hypothalamic-pituitary-thyroid axis [3]. Accumulating evidence showed that C-cells express thyrotropin releasing hormone (TRH) carrying out paracrine activity on follicular cells and inducing in them TRH-Rs expression [4]. In this way C cells are responsible for intrathyroidal regulation of follicular cells by permitting an interrelationship between the two endocrine populations [5]. Studies on the behavior of the thyroid C cells in follicular pathological conditions are contradictory. Maternal hypothyroidism induced by 131I leaded to the development of hyperplasia and hyperthrophy of calcitonin-positive cells in the pups at the time of birth [6]. Differently, hypothyroidism evoked by propylthiouracil attenuated density of parafollicular cells [7]. In addition less numerous C cells were found in simple and hyperactive goitre in comparison with normal thyroid parenchyma while proliferative changes concerned only follicular cells [8]. It is possible that the variance of results was due to greater complexity of theintrathyroidal regulatory pathway involving several C cell functions. Space missions are an excellent model to study the simultaneous changes in bone and follicular thyroid metabolism, both affected from C cells. In fact, spaceflight generated a skeletal adaptive response resulting in the loss of bone mass with the change of osteoblast differentiation and morphology [9], calcium metabolism and biochemical markers of bone turnover [10], bone formation and resorption processes [11]. Changes in blood flow, systemic hormones, and locally produced factors were indicated as important elements contributing to the response of osteoblastic cells to loading [9] but research in this field still has many questions. It has been demonstrated that in the longest mice permanence (91 days) on International Space Station (ISS) during the Mice Drawer System (MDS) mission, animals presented a bone loss but transgenic mice over-expressing pleiotrophin (PTNTG), molecule that produces positive effects on bone turnover, had an osteoblast activity higher than that observed in wild type (WT) mice, indicating that the expression of the PTN during the flight resulted in some protection against microgravity’s negative effects [12]. In the same experimental model, the structure of thyroid follicles appeared more organized, TSHR more expressed, cAMP release under TSH stimulation more intense in spaceflight mice than in control animals. The thyroid of PTN-TG mice was HIF-2��-IN-1 characterized by poorly developed follicles that were heterogeneous because of the variable size of both cells and colloid.Umus, Astrid Pouwelsen and Jacqueline Kuhnen for the breeding of the mosquitoes and Anja Scholzen and Chris Janse for critical revision of the manuscript.Author ContributionsConceived and designed the experiments: IHJP HJC. Performed the experiments: IHJP HJC MWR. Analyzed the data: IHJP. Contributed reagents/materials/analysis tools: HJC GJvG CCH MWR. Wrote the paper: IHJP RWS.
Parafollicular cells or Thyroid C cells are generally known for producing calcitonin, a hormone involved in calcium homeostasis with hypocalcemic and hypophosphatemic effects but it has been highlighted their role in the production of numerous regulatory peptides such as somatostatin and ghrelin [1], katacalcin I, katacalcin II, gastrin-releasing peptide, thyroliberin and helodermin [2]. Moreover C cells, under regulation by thyrotropin (TSH) because of TSH receptor (TSHR) expression, are involved in the hypothalamic-pituitary-thyroid axis [3]. Accumulating evidence showed that C-cells express thyrotropin releasing hormone (TRH) carrying out paracrine activity on follicular cells and inducing in them TRH-Rs expression [4]. In this way C cells are responsible for intrathyroidal regulation of follicular cells by permitting an interrelationship between the two endocrine populations [5]. Studies on the behavior of the thyroid C cells in follicular pathological conditions are contradictory. Maternal hypothyroidism induced by 131I leaded to the development of hyperplasia and hyperthrophy of calcitonin-positive cells in the pups at the time of birth [6]. Differently, hypothyroidism evoked by propylthiouracil attenuated density of parafollicular cells [7]. In addition less numerous C cells were found in simple and hyperactive goitre in comparison with normal thyroid parenchyma while proliferative changes concerned only follicular cells [8]. It is possible that the variance of results was due to greater complexity of theintrathyroidal regulatory pathway involving several C cell functions. Space missions are an excellent model to study the simultaneous changes in bone and follicular thyroid metabolism, both affected from C cells. In fact, spaceflight generated a skeletal adaptive response resulting in the loss of bone mass with the change of osteoblast differentiation and morphology [9], calcium metabolism and biochemical markers of bone turnover [10], bone formation and resorption processes [11]. Changes in blood flow, systemic hormones, and locally produced factors were indicated as important elements contributing to the response of osteoblastic cells to loading [9] but research in this field still has many questions. It has been demonstrated that in the longest mice permanence (91 days) on International Space Station (ISS) during the Mice Drawer System (MDS) mission, animals presented a bone loss but transgenic mice over-expressing pleiotrophin (PTNTG), molecule that produces positive effects on bone turnover, had an osteoblast activity higher than that observed in wild type (WT) mice, indicating that the expression of the PTN during the flight resulted in some protection against microgravity’s negative effects [12]. In the same experimental model, the structure of thyroid follicles appeared more organized, TSHR more expressed, cAMP release under TSH stimulation more intense in spaceflight mice than in control animals. The thyroid of PTN-TG mice was characterized by poorly developed follicles that were heterogeneous because of the variable size of both cells and colloid.