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Chung, Sungjin,Kim, Soojeong,Son, Mina,Kim, Minyoung,Koh, Eun Sil,Shin, Seok Joon,Park, Cheol Whee,Kim, Ho-Shik MDPI 2019 INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES Vol.20 No.7
<P>p300/CBP-associated factor (PCAF), a histone acetyltransferase, is involved in many cellular processes such as differentiation, proliferation, apoptosis, and reaction to cell damage by modulating the activities of several genes and proteins through the acetylation of either the histones or transcription factors. Here, we examined a pathogenic role of PCAF and its potential as a novel therapeutic target in the progression of renal tubulointerstitial fibrosis induced by non-diabetic unilateral ureteral obstruction (UUO) in male C57BL/6 mice. Administration of garcinol, a PCAF inhibitor, reversed a UUO-induced increase in the renal expression of total PCAF and histone 3 lysine 9 acetylation and reduced positive areas of trichrome and α-smooth muscle actin and collagen content. Treatment with garcinol also decreased mRNA levels of transforming growth factor-β, matrix metalloproteinase (MMP)-2, MMP-9, and fibronectin. Furthermore, garcinol suppressed nuclear factor-κB (NF-κB) and pro-inflammatory cytokines such as tumor necrosis factor-α and IL-6, whereas it preserved the nuclear expression of nuclear factor erythroid-derived 2-like factor 2 (Nrf2) and levels of Nrf2-dependent antioxidants including heme oxygense-1, catalase, superoxide dismutase 1, and NAD(P)H:quinone oxidoreductase 1. These results suggest that the inhibition of inordinately enhanced PCAF could mitigate renal fibrosis by redressing aberrant balance between inflammatory signaling and antioxidant response through the modulation of NF-κB and Nrf2.</P>
Urate Transporters in the Kidney: What Clinicians Need to Know
( Sungjin Chung ),( Gheun-ho Kim ) 대한전해질학회 2021 Electrolytes & Blood Pressure Vol.19 No.1
Urate is produced in the liver by the degradation of purines from the diet and nucleotide turnover and excreted by the kidney and gut. The kidney is the major route of urate removal and has a pivotal role in the regulation of urate homeostasis. Approximately 10% of the glomerular filtered urate is excreted in the urine, and the remainder is reabsorbed by the proximal tubule. However, the transport of urate in the proximal tubule is bidirectional: reabsorption and secretion. Thus, an increase in reabsorption or a decrease in secretion may induce hyperuricemia. In contrast, a decrease in reabsorption or an increase in secretion may result in hyperuricosuria. In the proximal tubule, urate reabsorption is mainly mediated by apical URAT1 (SLC22A12) and basolateral GLUT9 (SLC2A9) transporter. OAT4 (SLC22A11) also acts in urate reabsorption in the apical membrane, and its polymorphism is associated with the risk of hyperuricemia. Renal hypouricemia is caused by SLC22A12 or SLC2A9 loss-of-function mutations, and it may be complicated by exercise-induced acute kidney injury. URAT1 and GLUT9 are also drug targets for uricosuric agents. Sodium-glucose cotransporter inhibitors may induce hyperuricosuria by inhibiting GLUT9b located in the apical plasma membrane. Urate secretion is mediated by basolateral OAT1 (SLC22A6) and OAT3 (SLC22A8) and apical ATP-binding cassette super-family G member 2 (ABCG2), NPT1 (SLC17A1), and NPT4 (SLC17A3) transporter in the proximal tubule. NPT1 and NPT4 may be key players in renal urate secretion in humans, and deletion of SLC22A6 and SLC22A8 in mice leads to decreased urate excretion. Dysfunctional variants of ABCG2 inhibit urate secretion from the gut and kidney and may cause gout. In summary, the net result of urate transport in the proximal tubule is determined by the dominance of transporters between reabsorption (URAT1, OAT4, and GLUT9) and secretion (ABCG2, NPT1, NPT4, OAT1, and OAT3).
( Sungjin Chung ),( Mina Son ),( Yura Chae ),( Songhee Oh ),( Eun Sil Koh ),( Yong Kyun Kim ),( Seok Joon Shin ),( Cheol Whee Park ),( Sung-chul Jung ),( Ho-shik Kim ) 대한신장학회 2021 Kidney Research and Clinical Practice Vol.40 No.2
Background: Fabry disease is a rare X-linked genetic lysosomal disorder caused by mutations in the GLA gene encoding alpha-galactosidase A. Despite some data showing that profibrotic and proinflammatory cytokines and oxidative stress could be involved in Fabry disease-related renal injury, the pathogenic link between metabolic derangement within cells and renal injury remains unclear. Methods: Renal fibrosis was triggered by unilateral ureteral obstruction (UUO) in mice with Fabry disease to investigate the pathogenic mechanism leading to fibrosis in diseased kidneys. Results: Compared to kidneys of wild-type mice, lamellar inclusion bodies were recognized in proximal tubules of mice with Fabry disease. Sirius red and trichrome staining revealed significantly increased fibrosis in all UUO kidneys, though it was more prominent in obstructed Fabry kidneys. Renal messenger RNA levels of inflammatory cytokines and profibrotic factors were increased in all UUO kidneys compared to sham-operated kidneys but were not significantly different between UUO control and UUO Fabry mice. Protein levels of Nox2, Nox4, NQO1, catalase, SOD1, SOD2, and Nrf2 were not significantly different between UUO control and UUO Fabry kidneys, while the protein contents of LC3-II and LC3-I and expression of Beclin1 were significantly decreased in UUO kidneys of Fabry disease mouse models compared with wild-type mice. Notably, TUNEL-positive cells were elevated in obstructed kidneys of Fabry disease mice compared to wild-type control and UUO mice. Conclusion: These findings suggest that impaired autophagy and enhanced apoptosis are probable mechanisms involved in enhanced renal fibrosis under the stimulus of UUO in Fabry disease.
US28, a Virally-Encoded GPCR as an Antiviral Target for Human Cytomegalovirus Infection
( Sungjin Lee ),( Yoon Hee Chung ),( Choongho Lee ) 한국응용약물학회 2017 Biomolecules & Therapeutics(구 응용약물학회지) Vol.25 No.1
Viruses continue to evolve a new strategy to take advantage of every aspect of host cells in order to maximize their survival. Due to their central roles in transducing a variety of transmembrane signals, GPCRs seem to be a prime target for viruses to pirate for their own use. Incorporation of GPCR functionality into the genome of herpesviruses has been demonstrated to be essential for pathogenesis of many herpesviruses-induced diseases. Here, we introduce US28 of human cytomegalovirus (HCMV) as the best-studied example of virally-encoded GPCRs to manipulate host GPCR signaling. In this review, we wish to summarize a number of US28-related topics including its regulation of host signaling pathways, its constitutive internalization, its structural and functional analysis, its roles in HCMV biology and pathogenesis, its proliferative activities and role in oncogenesis, and pharmacological modulation of its biological activities. This review will aid in our understanding of how pathogenic viruses usurp the host GPCR signaling for successful viral infection. This kind of knowledge will enable us to build a better strategy to control viral infection by normalizing the virally-dysregulated host GPCR signaling.
관해유도 항암화학요법에 실패한 호지킨병 환자에서 2회의 자가 말초혈액 조혈모세포이식 후 지연되어 완전 관해된 1예
정성진,김일,박환철,오호석,최정혜,이영열,김인순,최일영,안명주 대한조혈모세포이식학회 2003 대한조혈모세포이식학회지 Vol.8 No.1
관해유도 항암화학요법에 실패한 호지킨병 환자에서 2회의 연속된 자가 조혈모세포이식은 하나의 치료 대안으로서 고려될 수 있다. 저자들은 진행된 호지킨병으로 진단된 뒤 기존 항암화학요법에 저항을 보여 자가 말초혈액 조혈모세포이식을 시행하였으나 여전히 부분 관해를 보였고, 재차 자가 말초혈액 조혈모세포이식을 시행하였으나 영상학적 검사에서 부분 관해에 머물렀던 환자가 조혈모세포 이식 3년 후 추적 검사에서는 완전 관해 소견을 보인 1예를 경험하여 이를 보고하는 바이다. The double autologous stem cell transplantation after high-dose therapy has been considered as a therapeutic chance for patients with refractory or relapsing Hodgkin's disease. We report here a 29-year-old patient with Hodgkin's disease (nodular sclerosis, Stage IVB), who was partially responsive to 6 cycles of conventional chemotherapy, achieved only partial remission despite double autologous peripheral blood stem cell transplantation. However, long- term follow-up with 3 years after second stem cell transplantation, the persistently remained tumors on spleen, left ilium, and right scapular area disappeared spontaneously and now the patient has no evidence of disease. Compared with previously reported cases of long-lasting persistent evidences of unresolved disease after allogeneic bone marrow transplantation with subsequent complete response in other hematologic malignancies, an atypical pattern in this case with delayed complete response after autologous hematopoietic stem cell transplantation has not been reported.
Performance analysis of packet errors on IEEE 802.11-based DCF and EDCF
Sungjin Shin,Jong-Moon Chung IET 2015 Electronics letters Vol.51 No.2
<P>The effect of packet size differences, that has not been taken into account in existing papers on the IEEE 802.11 distributed coordinated function (DCF) and 802.11e enhanced distributed coordinated function (EDCF), has been investigated, and improved throughput equations that lead to accurate performance representation in erroneous wireless channels are provided. Wi-Fi devices that use the DCF and the EDCF reduce the risk of data packet transmission failure using request to send (RTS) and clear to send (CTS) packets by removing the hidden node problem. However, as the bit error rate (BER) increases (especially near the signal coverage edge of the other communicating device), even though RTS/CTS packets may succeed in communication, data packets may fail due to packet errors based on their larger packet sizes. This phenomenon is confirmed through actual measurements and mathematical performance analysis is carried out to accurately express the performance of 802.11-based communications in erroneous conditions.</P>