FADD-deficient mouse embryonic fibroblasts undergo RIPK1-dependent apoptosis and autophagy after NB-UVB irradiation

Antunović, Maja; Matić, Igor; Nagy, Biserka; Mihalić, Katarina Caput; Skelin, Josipa; Štambuk, Jerko; Josipović, Pavle; Džinić, Tamara; Paradžik, Mladen; Marijanović, Inga

doi:10.1016/j.jphotobiol.2019.03.007

Cited by 7 publications

(11 citation statements)

References 56 publications

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“…A study demonstrates that miR-129-5p inhibits NP cell autophagy in IDD, and overexpression of miR-129-5p is beneficial for IDD treatment [11]. Fas-associated death domain (FADD) is not only a key adaptor protein in death receptor-mediated apoptosis, but also allimportant for successful conduction of apoptosis triggered with the absence of enrollment of death receptors, necrosis/necroptosis and autophagy [13]. Several articles have shown that the lack of FADD is connected with the proliferative benefit of cancer cells [14,15,].…”

Section: Introductionmentioning

confidence: 99%

RETRACTED ARTICLE: MicroRNA-129-5p affects immune privilege and apoptosis of nucleus pulposus cells via regulating FADD in intervertebral disc degeneration

Gao

Zhou

et al. 2020

Cell Cycle

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Literatures indicate that microRNA-129-5p (miR-129-5p) or Fas-associated death domain (FADD) is related to intervertebral disc degeneration (IDD), but the effect of miR-129-5p/FADD axis on IDD is not studied. The study aimed to investigate whether miR-129-5p influenced immune privilege and nucleus pulposus (NP) cell apoptosis in rats with IDD via regulating FADD.A rat model with caudal IDD was established, and injected with miR-129-5p agomir or miR-129-5p antagomir to figure out the character of miR-129-5p in the cell apoptosis and inflammation in the nucleus pulposus (NP) tissues of IDD rats. NP cells were grouped as the same ways for determining proliferation, apoptosis, and senescence in NP cells of IDD rats. Annexin V-FITC/PI double staining detected the apoptosis of macrophages and CD8 + cells co-cultured via transfected NP cells. Expression of miR-129-5p, FADD, collagen I, collagen II, aggrecan and Sox-9 in NP tissues and cells were determined.Up-regulated miR-129-5p decreased FADD, collagen I and elevated collagen Ⅱ, aggrecan, and Sox-9 in NP tissues and repressed inflammation in serum and NP tissues in IDD rats. Up-regulated miR-129-5p facilitated proliferation, inhibited senescence, apoptosis, and decreased FADD, collagen I and increased collagen Ⅱ, aggrecan, and Sox-9 in NP cells of IDD rats. Elevated miR-129-5p promoted the apoptosis of macrophages and CD8 + cells.We pronounced that up-regulated miR-129-5p inhibited the apoptosis and facilitated the proliferation of NP cells, as well as the apoptosis of macrophages and CD8 + cells via decreased FADD in IDD, suggesting that miR-129-5p had a protective effect on IDD.

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Section: Introductionmentioning

confidence: 99%

RETRACTED ARTICLE: MicroRNA-129-5p affects immune privilege and apoptosis of nucleus pulposus cells via regulating FADD in intervertebral disc degeneration

Gao

Zhou

et al. 2020

Cell Cycle

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“…Yang and Sun (13) validated BMP2 as a promoter of apoptosis and an inhibitor of NPC proliferation in IVDD, although it was also found to stimulate proteoglycan secretion to prevent the degradation of the ECM, which may help delay IVDD progression (13). Fas-associated death domain (FADD), an important agent for the triggering of cell death without the enrollment of death receptors, was also demonstrated to facilitate NPC apoptosis (132,133). Both BMP2 and FADD were confirmed to be targeted by miR-129-5p, and the overexpression of miR-129-5p was found to significantly facilitate the proliferation and suppress the apoptosis of NPCs (13).…”

Section: Diabetesmentioning

confidence: 99%

Role of microRNA‑129 in cancer and non‑cancerous diseases (Review)

2021

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An increasing number of studies indicate that microRNAs (miRNAs/miRs) are involved in diverse biological signaling pathways and play important roles in the progression of various diseases, including both oncological and non-oncological diseases. These small non-coding RNAs can block translation, resulting in a low expression level of target genes. miR-129 is an miRNA that has been the focus of considerable research in recent years. A growing body of evidence shows that the miR-129 family not only functions in cancer, including osteosarcoma, nasopharyngeal carcinoma, and ovarian, prostate, lung, breast and colon cancer, but also in non-cancerous diseases, including heart failure (HF), epilepsy, Alzheimer's disease (AD), obesity, diabetes and intervertebral disc degeneration (IVDD). It is therefore necessary to summarize current research progress on the role of miR-129 in different diseases. The present review includes an updated summary of the mechanisms of the miR-129 family in oncological and non-oncological diseases. To the best of our knowledge, this is the first review focusing on the role of miR-129 in non-cancerous diseases such as obesity, HF, epilepsy, diabetes, IVDD and AD. Contents 1. Introduction 2. Role of miR-129 in oncological phenotypes 3. Role of miR-129 in non-oncological phenotypes 4. Conclusion

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“…15,30 Moreover, necroptosis is associated with calpain activation. 31 Calpain is an enzyme that degrades proteins. Archana Shrestha et al showed that calpain inhibitors similarly blocked mixed-lineage kinase domain-like (MLKL) oligomerization induced by high concentrations of Clostridium perfringens enterotoxin (CPE), implicating calpain activation as a key intermediate in initiating CPEinduced necroptosis.…”

Section: Introduction To Necroptosismentioning

confidence: 99%

Research progress of keratinocyte‐programmed cell death in UV‐induced Skin photodamage

Tang

Tong

Huang

et al. 2021

Photoderm Photoimm Photomed

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Skin photodamage includes sunburn, phototoxic dermatitis, photosensitive dermatitis and photoaging. These common skin diseases that affect appearance are caused by ultraviolet radiation. The ultraviolet rays that reach the Earth are mainly divided into longwave ultraviolet rays (ultraviolet radiation A, UVA, 320 ~ 400 nm) and medium-wave ultraviolet rays (ultraviolet radiation B, UVB, 290 ~ 320 nm). UVA accounts for 95% of the ultraviolet radiation that reaches the Earth's surface 1 and leads to skin ageing and wrinkling because of cellular DNA damage by reactive oxygen species (ROS) production. 2,3 UVB is a major cause of skin reddening and sunburn through direct DNA damage. 3 Therefore, both types of UV radiation are chief causes of skin damage and can induce skin inflammation, ageing and eventually skin cancer. Human keratinocytes, as the outermost barrier of the skin, are the main target cells of UV radiation. Studies have shown that UV irradiation can induce different forms of programmed cell death (PCD) in keratinocytes, including apoptosis, pyroptosis, necroptosis and autophagy (Figure 1). In this review, we will briefly introduce the various types of PCD and their roles in UV-induced skin photodamage. | AP OP TOS IS | Introduction to apoptosisApoptosis is type of cell death in which the cell membrane remains intact. Apoptosis essentially does not induce inflammatory reactions. Initiator caspases (mainly caspase-2, −8, −9 and −10) and executioner caspases (such as caspase-3, −6 and −7) participate in the process of apoptosis. Apoptosis controls the development and homeostasis of multicellular organisms, and the distinct morphological characteristics of apoptosis are cell shrinkage and pyknosis,

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FADD-deficient mouse embryonic fibroblasts undergo RIPK1-dependent apoptosis and autophagy after NB-UVB irradiation

Cited by 7 publications

References 56 publications

RETRACTED ARTICLE: MicroRNA-129-5p affects immune privilege and apoptosis of nucleus pulposus cells via regulating FADD in intervertebral disc degeneration

RETRACTED ARTICLE: MicroRNA-129-5p affects immune privilege and apoptosis of nucleus pulposus cells via regulating FADD in intervertebral disc degeneration

Role of microRNA‑129 in cancer and non‑cancerous diseases (Review)

Research progress of keratinocyte‐programmed cell death in UV‐induced Skin photodamage

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