Cathelicidin promotes liver repair after acetaminophen-induced liver injury in mice

Zhai, Tingting; Zhang, Jingjing; Zhang, Jie; Liu, Bilian; Zhou, Zhiguang; Liu, Feng; Wu, Yan

doi:10.1016/j.jhepr.2023.100687

Cited by 11 publications

(6 citation statements)

References 40 publications

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“…So, lysosomal function is responsible for activating Nrf2 production through activating NR4A pathway, mediated by activating E coli proper functions, that will suppress the type I Interferonand. Also, Oxytocin alleviates liver fibrosis via hepatic macrophages [78]. And, inflammation upregulated OXTR transcription (as we mentioned previously) 10-to 250-fold relative to control in THP-1 and human primary macrophages and increased OXTR protein expression (mediated by promoting lysosomes and E coli functions) [79].…”

Section: That the Activation Of Inflammation In Patients Withsupporting

confidence: 53%

Decreasing in Lysine Reflect Lysosomal Dysfunction and Accumulated Phenylalanine which Connected to WMH and CVD and Both of Phenylketonuria and Calcifications where N-Acetylcysteine Prevent Organs Failure

M El Tantawi

2024

J Cardiol Res Rev Rep

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Phenylalanine function stabilized by lysine which found on lysosomal surface, that Phe necessary to regulate the synthesis or secretion of α-amylase, trypsin and lipase, where the Severe acute pancreatitis in a child with phenylketonuria. The phenylketonuria due to decreased lysine followed by lysosomal dysfunction that will be result of deficiency in phenylalanine function that will not form pancreatic enzymes and stomach enzyme and will be accumulated. The Lysosomal dysfunction will be result of accumulation of undigested polymer including inflammation which play important roles in pathophysiology, that reflect reduction in lysine acylation followed by reduction in aminoacyl tRNAs which promote Phe and E coli functions for activating protein and mRNAs synthesis, that will be followed by increasing in TNf-a synthesis (and reduction in VEGF-As ) which activate NK (not beings related to human immune proper function ) which regulated by the undigested polymers in random pathways stimulated by TNf-a functional pathway (activated by NLRP3 inflammasome. Retinoic acid is necessary to promote lysine acylation which regulate aminoacyl-tRNAs production regulated by mitochondrial enzymes, which regulate mRNA production by E coli (regulated by phenylalanine) that necessary to run antioxidant functions and cellular biosynthesis. Lysine acetylation so important to regulates the activity of Escherichia coli Sadenosylmethionine synthase. RNA (produced by E coli) is 2′-O-methylated demonstrated higher stability that can improve immune by promoting anti-inflammatory processes and improve myocardial functions, and adopt heart constriction by activating NR4As pathway. The antihypertensive pathway mechanism is: the Lysine ¬¬>activate ATPase (stimulate retinoic acid “RA” ) ¬¬>Lysine acetylation ¬¬> promote Phe/ hydroxylase ¬¬> followed by ¬>activate Tyr/ hydroxylase ¬>activate dopamine ¬> activate NR4As pathway ¬>GC-beta ¬>activate both of Oxytocin and Nrf2 ¬> Ang2-AT2 and VEGF-A productive functions ¬>heme oxygenase ¬>anti-inflammatory growth and processes. Lysine Methylation has important role in adopt hypertension through activating pervious Antihypertensive pathway mediated by Phe hydroxylase synthesis and Tyr hydroxylase production followed by activating both of dopamine and NR4As pathway. The oxidation of phenylalanyl-tRNA synthetase positively regulates translational quality control, and regulates the initiation of digestive enzyme mRNA translation, where consecutive AAA-lysines is paused for encoding Phe followed by ribosome sliding on homopolymeric A sequence. That lysine activates mitochondria function followed by promoting Phenylalanine and phenylalanine-tRNAs productions by translations within E coli, followed by Phe/ hydroxylase activate Tyr hydroxylase production which activate dopamine synthesis. And positively, Lysine is the most effective amino acid for activating all of ATPase, GTPase, and lysosomes, and E coli functions, where ATPase necessary for activating lysine Phosphorylation for activating lysosome digestion, followed by activating E coli through activating Phe hydroxylase production, while GTPase necessary for activating mitochondrial repairs, which act on pro-inflammation and cholesterol for activating estrogen production and activating the NR4As pathway which activate all of Oxytocin, Nrf2 followed by Ang2-AT2 and VEGF-A production and then followed by activating heme oxygenase and anti-inflammatory growth and processes that prevent LV-hypertrophy, and prevent coronary calcification.

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Section: That the Activation Of Inflammation In Patients Withsupporting

confidence: 53%

Decreasing in Lysine Reflect Lysosomal Dysfunction and Accumulated Phenylalanine which Connected to WMH and CVD and Both of Phenylketonuria and Calcifications where N-Acetylcysteine Prevent Organs Failure

M El Tantawi

2024

J Cardiol Res Rev Rep

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“…After the surgery, the mice were placed on a heating pad for recovering before being transferred back to the cage. In the second model, acetaminophen (PHx) was administered in 8-week male mice as previously described 21 , 22 . Briefly, the mice were fasted overnight (12–16 h) with free access to water.…”

Section: Methodsmentioning

confidence: 99%

Phosphatidic acid-enabled MKL1 contributes to liver regeneration: Translational implication in liver failure

Zhou,

Sun,

Chen

et al. 2024

Acta Pharmaceutica Sinica B

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“…Partial hepatectomy was performed as previously described [ 21 , 22 ]. Acetaminophen (APAP) was dissolved in 1XPBS and the mice received a single injection at a dose of 300 mg/kg as previously described [ 23 , 24 ]. Plasma LDH levels were measured using a commercially available kit (Abcam, ab102526) per vendor instructions.…”

Section: Methodsmentioning

confidence: 99%

TRIB1 regulates liver regeneration by antagonizing the NRF2-mediated antioxidant response

et al. 2023

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Robust regenerative response post liver injuries facilitates the architectural and functional recovery of the liver. Intrahepatic redox homeostasis plays a key role in liver regeneration. In the present study, we investigated the contributory role of Tribbles homolog 1 (Trib1), a pseudokinase, in liver regeneration and the underlying mechanism. We report that Trib1 expression was transiently down-regulated in animal and cell models of liver regeneration. Further analysis revealed that hepatocyte growth factor (HGF) repressed Trib1 transcription by evicting liver X receptor (LXRα) from the Trib1 promoter. Knockdown of Trib1 enhanced whereas over-expression of Trib1 suppressed liver regeneration after partial hepatectomy in mice. Of interest, regulation of liver regenerative response by Trib1 coincided with alterations of intracellular ROS levels, GSH levels, and antioxidant genes. Transcriptional assays suggested that Trib1 influenced cellular redox status by attenuating nuclear factor erythroid 2-related factor 2 (Nrf2) activity. Mechanistically, Trib1 interacted with the C-terminus of Nrf2 thus masking a potential nuclear localization signal (NLS) and blocking nuclear accumulation of Nrf2. Finally, correlation between Trib1 expression, Nrf2 nuclear localization, and cell proliferation was identified in liver specimens taken from patients with acute liver failure. In conclusion, our data unveil a novel pathway that depicts Trib1 as a critical link between intracellular redox homeostasis and cell proliferation in liver regeneration.

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Cathelicidin promotes liver repair after acetaminophen-induced liver injury in mice

Cited by 11 publications

References 40 publications

Decreasing in Lysine Reflect Lysosomal Dysfunction and Accumulated Phenylalanine which Connected to WMH and CVD and Both of Phenylketonuria and Calcifications where N-Acetylcysteine Prevent Organs Failure

Decreasing in Lysine Reflect Lysosomal Dysfunction and Accumulated Phenylalanine which Connected to WMH and CVD and Both of Phenylketonuria and Calcifications where N-Acetylcysteine Prevent Organs Failure

Phosphatidic acid-enabled MKL1 contributes to liver regeneration: Translational implication in liver failure

TRIB1 regulates liver regeneration by antagonizing the NRF2-mediated antioxidant response

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