Altered expression of p97/Valosin containing protein and impaired autophagy in preeclamptic human placenta

Özsoy, Asker Zeki; Çaylı, Sevil; Sahin, Cansu; Ocaklı, Seda; Sancı, Tuba Özdemir; Ilhan, Delibas Bahri

doi:10.1016/j.placenta.2018.05.013

Cited by 26 publications

(10 citation statements)

References 34 publications

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“…Dysregulated autophagy is involved in a large number of diseases such as neurodegenerative diseases and cancers. It is generally accepted that alteration of the autophagy activity is associated with the PE pathology; however, whether the autophagy activity is increased or impaired in the placenta of PE patients has been controversial (Oh et al, 2008;Chen et al, 2012;Akaishi et al, 2014;Saito and Nakashima, 2014;Gao et al, 2015;Melland-Smith et al, 2015;Zhang et al, 2016;Akcora Yildiz et al, 2017;Ozsoy et al, 2018). Most studies mainly focus on the detection of initial stage markers of autophagy pathways, such as LC3-II, Beclin-1, and SQSTM/P62, and suggest increased autophagy activity in the PE placenta.…”

Section: Autophagy and Inflammation In Pe Impaired Autophagy Linked To Pementioning

confidence: 99%

“…For instance, elevated expression of LC3 and Beclin-1 and reduced abundance of SQSTM1/p62 have been described in the placenta from PE women in comparison to normotensive controls (Oh et al, 2008;Gao et al, 2015;Melland-Smith et al, 2015). On the other hand, emerging evidence has shown the impairment of the autophagy-lysosomal pathway in the PE placenta (Saito and Nakashima, 2014;Ozsoy et al, 2018;Sharma, 2018;Nakashima et al, 2019b;Nakashima et al, 2020).…”

Section: Autophagy and Inflammation In Pe Impaired Autophagy Linked To Pementioning

confidence: 99%

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Etiological Value of Sterile Inflammation in Preeclampsia: Is It a Non-Infectious Pregnancy Complication?

Banerjee

Huang

Wang

et al. 2021

Front. Cell. Infect. Microbiol.

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Understanding of sterile inflammation and its associated biological triggers and diseases is still at the elementary stage. This becomes more warranted in cases where infections are not associated with the pathology. Detrimental effects of bacterial and viral infections on the immune responses at the maternal-fetal interface as well as pregnancy outcomes have been well documented. However, an infection-induced etiology is not thought to be a major contributing component to severe pregnancy complications such as preeclampsia (PE) and gestational diabetes. How is then an inflammatory signal thought to be associated with these pregnancy complications? It is not clear what type of inflammation is involved in the onset of PE-like features. We opine that sterile inflammation regulated by the inflammasome-gasdermins-caspase-1 axis is a contributory factor to the onset of PE. We hypothesize that increased production and release of damage-associated molecular patterns (DAMPs) or Alarmins such as high-mobility group box1 (HMGB1), cell-free fetal DNA, uric acid, the NOD-like receptor pyrin-containing receptor 3 (NLRP3) inflammasome, IL-1β and IL-18 occur in the PE placenta. Some of these molecules have already been observed in the placenta from women with PE. Mechanistically, emerging evidence has demonstrated that excessive placental endoplasmic reticulum (ER) stress, impaired autophagy and gasdermine D (GSDMD)-mediated intrinsic pyroptosis are key events that contribute to systemic sterile inflammation in patients with PE, especially early-onset PE (e-PE). In this review, we highlight the advances on the roles of sterile inflammation and inflammatory signaling cascades involving ER stress, autophagy deficiency and pyroptosis in PE pathophysiology. Deciphering the mechanisms underlying these inflammatory pathways may provide potential diagnostic biomarkers and facilitate the development of therapeutic strategies to treat this devastating disease.

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Section: Autophagy and Inflammation In Pe Impaired Autophagy Linked To Pementioning

confidence: 99%

Section: Autophagy and Inflammation In Pe Impaired Autophagy Linked To Pementioning

confidence: 99%

Etiological Value of Sterile Inflammation in Preeclampsia: Is It a Non-Infectious Pregnancy Complication?

Banerjee

Huang

Wang

et al. 2021

Front. Cell. Infect. Microbiol.

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“…Photographs were taken with a Leica microscope(Leica DM2500, Nussloch, Germany). H-SCORE analyses were used for the immunohistochemistry evaluation as previously described (15).…”

Section: Immunohistochemical Analysismentioning

confidence: 99%

Immunohistochemical examination of p97/VCP expression in developing mouse pancreas and liver

Kartal

Alimoğulları

Akcan

et al. 2021

Journal of Health Sciences and Medicine

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Aim:The 97-kDa Valosin-containing protein has important functions in proteolysis. Although the expression of p97/VCP has been studied in many types of cells and tissues, the localization of p97/VCP at cellular level in developing mouse pancreas and liver has not been determined. Therefore, the aim of our study was investigate the immuolocalization of p97/VCP in the mouse fetal and postnatal liver and pancreas. Material and Method: The liver and pancreas from fetal, postnatal (1, 5, 15, 35 days old ) and adult (50 days old) mice were examined by using immunohistochemistry in order to determine the expression of p97/VCP. Furthermore the development of mouse pancreas and liver were histomorphologically analyzed under light microscope. Results: The histological structures of the mouse pancreas and liver were maintained in postnatal period. The histological differences between endocrine and exocrine pancreas were significantly observed from the postnatal 5th day. The expression of p97/VCP in Langerhans islets was determined from day 5. p97/VCP expression was also seen in the exocrine pancreas in all postnatal days. p97/VCP was expressed in developing pancreatic and liver tissues and its expression was increased with the development. Conclusion:This study is the first to examine the distribution and the localization of p97/VCP in the fetal and postnatal mouse liver and pancreas. This study forms the basis for clinical studies in order to determine the function of p97/VCP in liver and pancreatic cells.

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“…Paradoxically, these changes may be derived from TFEB downregulation in preeclamptic placentas. In addition to the dysregulation of TFEB, decreases in p97/Valosin-containing protein, which is a member of the ATPase associated protein family, might mediate autophagy inhibition in preeclamptic placentas [74]. Mutations in the p97/Valosin-containing protein, which is involved in a variety of cellular functions including autophagy, ER stress response, endosomal trafficking, cell cycle, and DNA repair, have also been shown to be related to the development of several degenerative diseases, including frontotemporal dementia and amyotrophic lateral sclerosis [75].…”

Section: Lysosomal Dysregulation In Preeclampsiamentioning

confidence: 99%

Disruption of Placental Homeostasis Leads to Preeclampsia

Nakashima

Saito

Tsuda

et al. 2020

IJMS

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Placental homeostasis is directly linked to fetal well-being and normal fetal growth. Placentas are sensitive to various environmental stressors, including hypoxia, endoplasmic reticulum stress, and oxidative stress. Once placental homeostasis is disrupted, the placenta may rebel against the mother and fetus. Autophagy is an evolutionally conservative mechanism for the maintenance of cellular and organic homeostasis. Evidence suggests that autophagy plays a crucial role throughout pregnancy, including fertilization, placentation, and delivery in human and mouse models. This study reviews the available literature discussing the role of autophagy in preeclampsia.

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Altered expression of p97/Valosin containing protein and impaired autophagy in preeclamptic human placenta

Cited by 26 publications

References 34 publications

Etiological Value of Sterile Inflammation in Preeclampsia: Is It a Non-Infectious Pregnancy Complication?

Etiological Value of Sterile Inflammation in Preeclampsia: Is It a Non-Infectious Pregnancy Complication?

Immunohistochemical examination of p97/VCP expression in developing mouse pancreas and liver

Disruption of Placental Homeostasis Leads to Preeclampsia

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