Necroptosis mediated by receptor interacting protein kinase 3 as critical players in experimental congenital hypothyroidism related neuronal damage

Yavuz, Hayrettin; Alcigir, Mehmet Eray; Duman, Gülhan

doi:10.14744/nci.2021.26043

Necroptosis mediated by receptor interacting protein kinase 3 as critical players in experimental congenital hypothyroidism related neuronal damage

Gülhan DUMAN, (Department of Endocrinology and Metabolic Disorders, Sivas Cumhuriyet University Faculty of Medicine, Sivas, Türkiye)

MEHMET ERAY ALÇIĞIR, (Department of Pathology, Kirikkale University Faculty of Veterinary Medicine, Kirikkale, Türkiye)

Hayrettin YAVUZ (Department of Biochemistry, Sivas Cumhuriyet University Faculty of Medicine, Sivas, Türkiye)

İstanbul Kuzey Klinikleri

4 0

Yıl: 2021 Cilt: 8 Sayı: 5 Sayfa Aralığı: 472 - 478 Metin Dili: İngilizce DOI: 10.14744/nci.2021.26043 İndeks Tarihi: 24-05-2022

Necroptosis mediated by receptor interacting protein kinase 3 as critical players in experimental congenital hypothyroidism related neuronal damage

Öz:

OBJECTIVE: Congenital hypothyroidism (CH) is literally described as congenital thyroid hormone imperfection. The primary objective of this research was to reveal the possible relation between receptor-acting protein kinase 3 (RIPK3) activity and neuronal damages in rat pups with CH. In addition, we evaluated the favorable impacts of 3.6-dibromo-α-([phenylamino] methyl)-9H-carbazole-9-ethanol (P7C3) reducing RIPK3 activity. METHODS: Adult rats were accordingly assigned into four groups: Group 1, which is called congenital hypothyroid; Group 2, which is called congenital hypothyroid administered P7C3; Group 3, called CH administered P7C3 and L-thyroxine; and Group 4, control group. RIPK3 level in plasma concentration and its expression in tissue was determined in all groups. RESULTS: Increased RIPK3 expressions were detected as high in the CH group when it is compared to the control group. Furthermore; the expressions in neuronal cytoplasm were found similar among Groups II and III. RIPK3 expressions in those two groups were relatively higher than in the control group. Most reacted parts of the brain were especially Purkinje cells in the cerebellum. CONCLUSION: It is concluded that there is excellent parallelism among damaged neurons and high RIPK3 activity in CH pathogenesis. P7C3 compounds may have a safeguarding impact on CH due to decreasing RIPK3 activity.

Anahtar Kelime:

Belge Türü: Makale Makale Türü: Araştırma Makalesi Erişim Türü: Erişime Açık

1.van Tellingen V, Finken MJ, Israëls J, Hendriks YM, Kamp GA, van Santen HM. Poorly controlled congenital hypothyroidism due to an underlying allgrove syndrome. Horm Res Paediatr 2016;86:420–4.
2. Powell MH, Nguyen HV, Gilbert M, Parekh M, Colon-Perez LM, Mareci TH, et al. Magnetic resonance imaging and volumetric analysis: novel tools to study the effects of thyroid hormone disruption on white matter development. Neurotoxicology 2012;33:1322–9.
3. Moog NK, Entringer S, Heim C, Wadhwa PD, Kathmann N, Buss C. Influence of maternal thyroid hormones during gestation on fetal brain development. Neuroscience 2017;342:68–100.
4. Gilbert ME, Rovet J, Chen Z, Koibuchi N. Developmental thyroid hormone disruption: prevalence, environmental contaminants and neurodevelopmental consequences. Neurotoxicology 2012;33:842–52.
5. Toft AD. Thyroxine therapy. N Engl J Med 1994;331:174–80.
6. Pieper AA, McKnight SL, Ready JM. P7C3 and an unbiased approach to drug discovery for neurodegenerative diseases. Chem Soc Rev 2014;43:6716–26.
7. Bauman MD, Schumann CM, Carlson EL, Tayor SL, Vázquez-Rosa E, Cintrón-Pérez CJ, et al. Neuroprotective efficacy of P7C3 compounds in primate hippocampus. Transl Psychiatry 2018;8:202.
8. Voorhees JR, Remy MT, Cintrón-Pérez CJ, El Rassi E, Khan MZ, Dutca LM, et al. (-)-P7C3-S243 protects a rat model of Alzheimer’s disease from neuropsychiatric deficits and neurodegeneration without altering amyloid deposition or reactive glia. Biol Psychiatry 2018;84:488–98.
9. Dogan HO, Alcigir ME. The protective effect of P7C3 against DNA and neuron damage in rat pups with congenital hypothyroidism. Biomed Pharmacother 2018;99:499–503.
10. Golstein P, Kroemer G. Cell death by necrosis: towards a molecular definition. Trends Biochem Sci 2007;32:37–43.
11. Kroemer G, Galluzzi L, Vandenabeele P, Abrams J, Alnemri ES, Baehrecke EH, et al; Nomenclature Committee on Cell Death 2009. Classification of cell death: recommendations of the Nomenclature Committee on Cell Death 2009. Cell Death Differ 2009;16:3–11.
12. Re DB, Le Verche V, Yu C, Amoroso MW, Politi KA, Phani S, et al. Necroptosis drives motor neuron death in models of both sporadic and familial ALS. Neuron 2014;81:1001–8.
13. Vitner EB, Salomon R, Farfel-Becker T, Meshcheriakova A, Ali M, Klein AD, et al. RIPK3 as a potential therapeutic target for Gaucher’s disease. Nat Med 2014;20:204–8.
14. Ofengeim D, Ito Y, Najafov A, Zhang Y, Shan B, DeWitt JP, et al. Activation of necroptosis in multiple sclerosis. Cell Rep 2015;10:1836–49.
15. Caccamo A, Branca C, Piras IS, Ferreira E, Huentelman MJ, Liang WS, et al. Necroptosis activation in Alzheimer’s disease. Nat Neurosci 2017;20:1236–46.
16. Yang J, Zhao Y, Zhang L, Fan H, Qi C, Zhang K, et al. RIPK3/MLKLMediated Neuronal Necroptosis Modulates the M1/M2 Polarization of Microglia/Macrophages in the Ischemic Cortex. Cereb Cortex 2018;28:2622–35.
17. Yang M, Lv Y, Tian X, Lou J, An R, Zhang Q, et al. Neuroprotective effect of β-caryophyllene on cerebral ischemia-reperfusion injury via regulation of necroptotic neuronal death and inflammation: in vivo and in vitro. Front Neurosci 2017;11:583.
18. Qinli Z, Meiqing L, Xia J, Li X, Weili G, Xiuliang J, et al. Necrostatin-1 inhibits the degeneration of neural cells induced by aluminum exposure. Restor Neurol Neurosci 2013;31:543–55.
19. Mohan V, Sinha RA, Pathak A, Rastogi L, Kumar P, Pal A, et al. Maternal thyroid hormone deficiency affects the fetal neocorticogenesis by reducing the proliferating pool, rate of neurogenesis and indirect neurogenesis. Exp Neurol 2012;237:477–88.
20. Domingues JT, Wajima CS, Cesconetto PA, Parisotto EB, Winkelmann- Duarte E, Santos KD, et al. Experimentally-induced maternal hypothyroidism alters enzyme activities and the sensorimotor cortex of the offspring rats. Mol Cell Endocrinol 2018;478:62–76.
21. Amano I, Takatsuru Y, Toya S, Haijima A, Iwasaki T, Grasberger H, et al. Aberrant cerebellar development in mice lacking dual oxidase maturation factors. Thyroid 2016;26:741–52.
22. Salami M, Bandegi AR, Sameni HR, Vafaei AA, Pakdel A. Hippocampal up-regulation of apolipoprotein d in a rat model of maternal hypoand hyperthyroidism: implication of oxidative stress. Neurochem Res 2019;44:2190–201.
23. Ahmed OM, Ahmed RG, El-Gareib AW, El-Bakry AM, Abd El-Tawab SM. Effects of experimentally induced maternal hypothyroidism and hyperthyroidism on the development of rat offspring: II-the developmental pattern of neurons in relation to oxidative stress and antioxidant defense system. Int J Dev Neurosci 2012;30:517–37.
24. Cattani D, Goulart PB, Cavalli VL, Winkelmann-Duarte E, Dos Santos AQ, Pierozan P, et al. Congenital hypothyroidism alters the oxidative status, enzyme activities and morphological parameters in the hippocampus of developing rats. Mol Cell Endocrinol 2013;375:14–26.
25. Belenky P, Bogan KL, Brenner C. NAD+ metabolism in health and disease. Trends Biochem Sci 2007;32:12–9.
26. Masullo LF, Magalhães RA, Lemes RPG, de Almeida Filho TP, de Castro MF, Maia Filho PA, et al. Levothyroxine replacement improves oxidative status in primary hypothyroidism. Front Endocrinol (Lausanne) 2018;9:655.
27. Ates I, Altay M, Yilmaz FM, Topcuoglu C, Yilmaz N, Berker D, et al. The impact of levothyroxine sodium treatment on oxidative stress in Hashimoto’s thyroiditis. Eur J Endocrinol 2016;174:727–34.

APA	Duman G, Alcigir M, Yavuz H (2021). Necroptosis mediated by receptor interacting protein kinase 3 as critical players in experimental congenital hypothyroidism related neuronal damage. , 472 - 478. 10.14744/nci.2021.26043
Chicago	Duman Gülhan,Alcigir Mehmet Eray,Yavuz Hayrettin Necroptosis mediated by receptor interacting protein kinase 3 as critical players in experimental congenital hypothyroidism related neuronal damage. (2021): 472 - 478. 10.14744/nci.2021.26043
MLA	Duman Gülhan,Alcigir Mehmet Eray,Yavuz Hayrettin Necroptosis mediated by receptor interacting protein kinase 3 as critical players in experimental congenital hypothyroidism related neuronal damage. , 2021, ss.472 - 478. 10.14744/nci.2021.26043
AMA	Duman G,Alcigir M,Yavuz H Necroptosis mediated by receptor interacting protein kinase 3 as critical players in experimental congenital hypothyroidism related neuronal damage. . 2021; 472 - 478. 10.14744/nci.2021.26043
Vancouver	Duman G,Alcigir M,Yavuz H Necroptosis mediated by receptor interacting protein kinase 3 as critical players in experimental congenital hypothyroidism related neuronal damage. . 2021; 472 - 478. 10.14744/nci.2021.26043
IEEE	Duman G,Alcigir M,Yavuz H "Necroptosis mediated by receptor interacting protein kinase 3 as critical players in experimental congenital hypothyroidism related neuronal damage." , ss.472 - 478, 2021. 10.14744/nci.2021.26043
ISNAD	Duman, Gülhan vd. "Necroptosis mediated by receptor interacting protein kinase 3 as critical players in experimental congenital hypothyroidism related neuronal damage". (2021), 472-478. https://doi.org/10.14744/nci.2021.26043

APA	Duman G, Alcigir M, Yavuz H (2021). Necroptosis mediated by receptor interacting protein kinase 3 as critical players in experimental congenital hypothyroidism related neuronal damage. İstanbul Kuzey Klinikleri, 8(5), 472 - 478. 10.14744/nci.2021.26043
Chicago	Duman Gülhan,Alcigir Mehmet Eray,Yavuz Hayrettin Necroptosis mediated by receptor interacting protein kinase 3 as critical players in experimental congenital hypothyroidism related neuronal damage. İstanbul Kuzey Klinikleri 8, no.5 (2021): 472 - 478. 10.14744/nci.2021.26043
MLA	Duman Gülhan,Alcigir Mehmet Eray,Yavuz Hayrettin Necroptosis mediated by receptor interacting protein kinase 3 as critical players in experimental congenital hypothyroidism related neuronal damage. İstanbul Kuzey Klinikleri, vol.8, no.5, 2021, ss.472 - 478. 10.14744/nci.2021.26043
AMA	Duman G,Alcigir M,Yavuz H Necroptosis mediated by receptor interacting protein kinase 3 as critical players in experimental congenital hypothyroidism related neuronal damage. İstanbul Kuzey Klinikleri. 2021; 8(5): 472 - 478. 10.14744/nci.2021.26043
Vancouver	Duman G,Alcigir M,Yavuz H Necroptosis mediated by receptor interacting protein kinase 3 as critical players in experimental congenital hypothyroidism related neuronal damage. İstanbul Kuzey Klinikleri. 2021; 8(5): 472 - 478. 10.14744/nci.2021.26043
IEEE	Duman G,Alcigir M,Yavuz H "Necroptosis mediated by receptor interacting protein kinase 3 as critical players in experimental congenital hypothyroidism related neuronal damage." İstanbul Kuzey Klinikleri, 8, ss.472 - 478, 2021. 10.14744/nci.2021.26043
ISNAD	Duman, Gülhan vd. "Necroptosis mediated by receptor interacting protein kinase 3 as critical players in experimental congenital hypothyroidism related neuronal damage". İstanbul Kuzey Klinikleri 8/5 (2021), 472-478. https://doi.org/10.14744/nci.2021.26043