Background and Summary: We review the transcriptional regulation of ABO expression and discuss variants in the promoter and erythroid cell-specific regulatory region in individuals with weak ABO phenotypes such as Bm, Am, B3, and A3. We also review the molecular mechanisms responsible for variations in ABO expression in development and disease including the cell type-specific expression of ABO during erythroid cell differentiation, and reduction of A- or B-antigens in cancer cells or on red blood cells in patients with leukemia. Although the relationship between ABO blood group antigens and diseases has been characterized, the physiological significance of the ABO blood group system remains unclear. Key Messages: This review discusses accumulated knowledge of the ABO gene regulation and potential reasons for conservation of ABO during evolution.
{"title":"Review of ABO Expression and Variations based on Transcriptional Regulation of the ABO Blood Group Gene","authors":"Kenichi Ogasawara, R. Sano, Y. Kominato","doi":"10.1159/000536556","DOIUrl":"https://doi.org/10.1159/000536556","url":null,"abstract":"<b><i>Background and Summary:</i></b> We review the transcriptional regulation of <i>ABO</i> expression and discuss variants in the promoter and erythroid cell-specific regulatory region in individuals with weak ABO phenotypes such as B<sub>m</sub>, A<sub>m</sub>, B<sub>3</sub>, and A<sub>3</sub>. We also review the molecular mechanisms responsible for variations in <i>ABO</i> expression in development and disease including the cell type-specific expression of <i>ABO</i> during erythroid cell differentiation, and reduction of A- or B-antigens in cancer cells or on red blood cells in patients with leukemia. Although the relationship between ABO blood group antigens and diseases has been characterized, the physiological significance of the ABO blood group system remains unclear. <b><i>Key Messages:</i></b> This review discusses accumulated knowledge of the <i>ABO</i> gene regulation and potential reasons for conservation of ABO during evolution.","PeriodicalId":505859,"journal":{"name":"Transfusion Medicine and Hemotherapy","volume":"89 4","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-03-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140249580","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Background: Pathogen inactivation treatment (PIT) has been shown to alter platelet function, phenotype, morphology and to induce a faster aging of platelet concentrates (PCs). Key pieces of information are still missing to understand the impacts of PITs at the cellular level. Objectives: This study investigated the impact of amotosalen/UVA on PCs, from a post-translational modifications (PTM) point of view. Phosphoproteomic analyses were conducted on resting platelets, right after the amotosalen/UVA treatment and compared with untreated PCs. Method: A two-arm study setting was carried out to compare PIT (amotosalen/UVA) to untreated PCs, on day 1 post-donation. Based on a pool-and-split approach, 12 PCs were split into two groups (treated and untreated). Quantitative phosphoproteomics was performed using TMT technology to study the changes of phosphoproteins right after the PIT. Results: A total of 3,906 proteins and 7,334 phosphosites were identified, and 2,473 proteins and 2,214 phosphosites were observed in at least 5 to 6 replicates. Compared to untreated platelets, PIT platelets exhibited an upregulation of the phosphorylation effects, with 109 phosphosites identified with a higher than 2-fold change. Two pathways were clearly identified. The mitogen activated protein kinases (MAPKs) cascade, which triggers the granule secretion and the activation of the pS15 HSPB1. One of the shape change pathways was also observed with the inhibition of the Threonine 18 and Serine 19 phosphorylations on myosin light chain (MLC) protein after the amotosalen/UVA treatment. Conclusions: This work provides a deep insight into the impact of amotosalen/UVA treatment from a phosphoprotein viewpoint on resting platelets. Clear changes in phosphorylation of proteins belonging to different platelet pathways were quantified. This discovery corroborates previous findings and fills missing parts of the effect of photochemical treatments on platelets.
{"title":"Increase of Phosphoprotein Expressions in Amotosalen/UVA-Treated Platelet Concentrates","authors":"C. Muret, D. Crettaz, Lorenzo Alberio, M. Prudent","doi":"10.1159/000535060","DOIUrl":"https://doi.org/10.1159/000535060","url":null,"abstract":"Background: Pathogen inactivation treatment (PIT) has been shown to alter platelet function, phenotype, morphology and to induce a faster aging of platelet concentrates (PCs). Key pieces of information are still missing to understand the impacts of PITs at the cellular level. Objectives: This study investigated the impact of amotosalen/UVA on PCs, from a post-translational modifications (PTM) point of view. Phosphoproteomic analyses were conducted on resting platelets, right after the amotosalen/UVA treatment and compared with untreated PCs. Method: A two-arm study setting was carried out to compare PIT (amotosalen/UVA) to untreated PCs, on day 1 post-donation. Based on a pool-and-split approach, 12 PCs were split into two groups (treated and untreated). Quantitative phosphoproteomics was performed using TMT technology to study the changes of phosphoproteins right after the PIT. Results: A total of 3,906 proteins and 7,334 phosphosites were identified, and 2,473 proteins and 2,214 phosphosites were observed in at least 5 to 6 replicates. Compared to untreated platelets, PIT platelets exhibited an upregulation of the phosphorylation effects, with 109 phosphosites identified with a higher than 2-fold change. Two pathways were clearly identified. The mitogen activated protein kinases (MAPKs) cascade, which triggers the granule secretion and the activation of the pS15 HSPB1. One of the shape change pathways was also observed with the inhibition of the Threonine 18 and Serine 19 phosphorylations on myosin light chain (MLC) protein after the amotosalen/UVA treatment. Conclusions: This work provides a deep insight into the impact of amotosalen/UVA treatment from a phosphoprotein viewpoint on resting platelets. Clear changes in phosphorylation of proteins belonging to different platelet pathways were quantified. This discovery corroborates previous findings and fills missing parts of the effect of photochemical treatments on platelets.","PeriodicalId":505859,"journal":{"name":"Transfusion Medicine and Hemotherapy","volume":"55 12","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-02-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139849287","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Background: Pathogen inactivation treatment (PIT) has been shown to alter platelet function, phenotype, morphology and to induce a faster aging of platelet concentrates (PCs). Key pieces of information are still missing to understand the impacts of PITs at the cellular level. Objectives: This study investigated the impact of amotosalen/UVA on PCs, from a post-translational modifications (PTM) point of view. Phosphoproteomic analyses were conducted on resting platelets, right after the amotosalen/UVA treatment and compared with untreated PCs. Method: A two-arm study setting was carried out to compare PIT (amotosalen/UVA) to untreated PCs, on day 1 post-donation. Based on a pool-and-split approach, 12 PCs were split into two groups (treated and untreated). Quantitative phosphoproteomics was performed using TMT technology to study the changes of phosphoproteins right after the PIT. Results: A total of 3,906 proteins and 7,334 phosphosites were identified, and 2,473 proteins and 2,214 phosphosites were observed in at least 5 to 6 replicates. Compared to untreated platelets, PIT platelets exhibited an upregulation of the phosphorylation effects, with 109 phosphosites identified with a higher than 2-fold change. Two pathways were clearly identified. The mitogen activated protein kinases (MAPKs) cascade, which triggers the granule secretion and the activation of the pS15 HSPB1. One of the shape change pathways was also observed with the inhibition of the Threonine 18 and Serine 19 phosphorylations on myosin light chain (MLC) protein after the amotosalen/UVA treatment. Conclusions: This work provides a deep insight into the impact of amotosalen/UVA treatment from a phosphoprotein viewpoint on resting platelets. Clear changes in phosphorylation of proteins belonging to different platelet pathways were quantified. This discovery corroborates previous findings and fills missing parts of the effect of photochemical treatments on platelets.
{"title":"Increase of Phosphoprotein Expressions in Amotosalen/UVA-Treated Platelet Concentrates","authors":"C. Muret, D. Crettaz, Lorenzo Alberio, M. Prudent","doi":"10.1159/000535060","DOIUrl":"https://doi.org/10.1159/000535060","url":null,"abstract":"Background: Pathogen inactivation treatment (PIT) has been shown to alter platelet function, phenotype, morphology and to induce a faster aging of platelet concentrates (PCs). Key pieces of information are still missing to understand the impacts of PITs at the cellular level. Objectives: This study investigated the impact of amotosalen/UVA on PCs, from a post-translational modifications (PTM) point of view. Phosphoproteomic analyses were conducted on resting platelets, right after the amotosalen/UVA treatment and compared with untreated PCs. Method: A two-arm study setting was carried out to compare PIT (amotosalen/UVA) to untreated PCs, on day 1 post-donation. Based on a pool-and-split approach, 12 PCs were split into two groups (treated and untreated). Quantitative phosphoproteomics was performed using TMT technology to study the changes of phosphoproteins right after the PIT. Results: A total of 3,906 proteins and 7,334 phosphosites were identified, and 2,473 proteins and 2,214 phosphosites were observed in at least 5 to 6 replicates. Compared to untreated platelets, PIT platelets exhibited an upregulation of the phosphorylation effects, with 109 phosphosites identified with a higher than 2-fold change. Two pathways were clearly identified. The mitogen activated protein kinases (MAPKs) cascade, which triggers the granule secretion and the activation of the pS15 HSPB1. One of the shape change pathways was also observed with the inhibition of the Threonine 18 and Serine 19 phosphorylations on myosin light chain (MLC) protein after the amotosalen/UVA treatment. Conclusions: This work provides a deep insight into the impact of amotosalen/UVA treatment from a phosphoprotein viewpoint on resting platelets. Clear changes in phosphorylation of proteins belonging to different platelet pathways were quantified. This discovery corroborates previous findings and fills missing parts of the effect of photochemical treatments on platelets.","PeriodicalId":505859,"journal":{"name":"Transfusion Medicine and Hemotherapy","volume":" 2","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-02-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139789575","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"A Call to Reinvent Platelet Products","authors":"S. Handtke, Thomas Thiele","doi":"10.1159/000536237","DOIUrl":"https://doi.org/10.1159/000536237","url":null,"abstract":"","PeriodicalId":505859,"journal":{"name":"Transfusion Medicine and Hemotherapy","volume":"39 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-02-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139854974","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"A Call to Reinvent Platelet Products","authors":"S. Handtke, Thomas Thiele","doi":"10.1159/000536237","DOIUrl":"https://doi.org/10.1159/000536237","url":null,"abstract":"","PeriodicalId":505859,"journal":{"name":"Transfusion Medicine and Hemotherapy","volume":"7 22","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-02-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139795208","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Xin Dai, Chengcheng Liu, Rong Chen, Ting Jiang, Ruoyang Zhang, Chenchen Feng, Taixiang Liu, Hong Lü, Wenbiao Liang
Introduction: This study aimed to investigate the allele frequencies of the human platelet antigens (HPA) HPA-1-29w system in Jiangsu (China) and establish the platelet apheresis registry in blood donors. Methods: HPA genotyping was performed using the MassARRAY iPLEX® platform. Allele and genotype frequencies were estimated by direct counting and tested for Hardy-Weinberg equilibrium. The transfusion mismatch probability was calculated for every HPA specificity. Results: The HPA allele frequencies in the Jiangsu Han population of HPA-1b, -2b, -3b, -4b, -5b, -6b, -11b, -15b, and -21b were 0.0055, 0.0530, 0.4116, 0.0015, 0.0155, 0.0162, 0.0003, 0.4683, and 0.0070, respectively, in which a heterozygote of HPA-11a/b was first detected in China. Only allele a was detected for HPA-7-10w,-12-14w,-16-20w, and -22-29w quasi-systems. The highest mismatch rate of HPA genes in 1,640 platelet donors was the HPA-15 system, followed by the HPA-3 system with a rate of 37.4% and 36.71%, respectively. Conclusion: China’s largest-scale platelet registry of HPA-1-29w has been explored. The MassARRAY platform may help found the platelet apheresis registry which would be useful to provide matching platelets and lead to a more accurate, effective, and safe transfusion for patients with platelet therapy.
{"title":"HPA1-29w Genotyping and the Foundation for the Platelet Apheresis Registry in Jiangsu Province of China by MassARRAY Spectrometry","authors":"Xin Dai, Chengcheng Liu, Rong Chen, Ting Jiang, Ruoyang Zhang, Chenchen Feng, Taixiang Liu, Hong Lü, Wenbiao Liang","doi":"10.1159/000535653","DOIUrl":"https://doi.org/10.1159/000535653","url":null,"abstract":"Introduction: This study aimed to investigate the allele frequencies of the human platelet antigens (HPA) HPA-1-29w system in Jiangsu (China) and establish the platelet apheresis registry in blood donors. Methods: HPA genotyping was performed using the MassARRAY iPLEX® platform. Allele and genotype frequencies were estimated by direct counting and tested for Hardy-Weinberg equilibrium. The transfusion mismatch probability was calculated for every HPA specificity. Results: The HPA allele frequencies in the Jiangsu Han population of HPA-1b, -2b, -3b, -4b, -5b, -6b, -11b, -15b, and -21b were 0.0055, 0.0530, 0.4116, 0.0015, 0.0155, 0.0162, 0.0003, 0.4683, and 0.0070, respectively, in which a heterozygote of HPA-11a/b was first detected in China. Only allele a was detected for HPA-7-10w,-12-14w,-16-20w, and -22-29w quasi-systems. The highest mismatch rate of HPA genes in 1,640 platelet donors was the HPA-15 system, followed by the HPA-3 system with a rate of 37.4% and 36.71%, respectively. Conclusion: China’s largest-scale platelet registry of HPA-1-29w has been explored. The MassARRAY platform may help found the platelet apheresis registry which would be useful to provide matching platelets and lead to a more accurate, effective, and safe transfusion for patients with platelet therapy.","PeriodicalId":505859,"journal":{"name":"Transfusion Medicine and Hemotherapy","volume":"8 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-01-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139525137","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Hyungsuk Kim, Kyunghoon Lee, Soo Hyun Seo, Y. J. Hong, Sang Mee Hwang, Jeong Su Park, Kyoung Un Park, Junghan Song
Introduction: Di(2-ethylhexyl) phthalate (DEHP) is a plasticizer commonly used in blood bags. Despite its protective effects on red blood cell (RBC) storage, concerns about its reproductive toxicity exist. This study investigated the in vitro quality of RBC concentrates stored in bags using di(isononyl) cyclohexane-1,2-dicarboxylate (DINCH) as an alternative plasticizer. Methods: Using a pool-and-split study design, we produced 20 matched homogenous quintets of RBC concentrates in two DINCH bags and three DEHP bags with citrate phosphate dextrose adenine (CPDA-1) anticoagulant. RBC storage quality was assessed weekly for 35 days. Results: On day 35, the median hemolysis levels in the DINCH bags (0.297–0.342%) were marginally higher (p < 0.05) than the DEHP bags (0.204–0.240%). All DINCH bags showed <0.8% hemolysis. RBCs in the DINCH bags showed increased mean corpuscular volume and decreased eosin 5′ maleimide binding than in the DEHP bags. Higher pO2 and lower pCO2 levels in the DINCH bags indicated better gas permeability than in DEHP bags. Other metabolic parameters were comparable in both bags. Compared to DEHP, DINCH exhibited considerably lower levels of plasticizer leaching into blood bags. Conclusion: The quality of RBC concentrates stored for 35 days in DINCH-plasticized blood bags with CDPA-1 is generally comparable to those in DEHP bags. Hence, DINCH can be a viable alternative to DEHP in blood bags for nonleukoreduced RBC storage even without the use of next-generation additive solutions to improve RBC preservation quality.
{"title":"In vitro Evaluation of DINCH-Plasticized Blood Bags for Red Blood Cell Storage with CPDA-1 Anticoagulant","authors":"Hyungsuk Kim, Kyunghoon Lee, Soo Hyun Seo, Y. J. Hong, Sang Mee Hwang, Jeong Su Park, Kyoung Un Park, Junghan Song","doi":"10.1159/000535625","DOIUrl":"https://doi.org/10.1159/000535625","url":null,"abstract":"Introduction: Di(2-ethylhexyl) phthalate (DEHP) is a plasticizer commonly used in blood bags. Despite its protective effects on red blood cell (RBC) storage, concerns about its reproductive toxicity exist. This study investigated the in vitro quality of RBC concentrates stored in bags using di(isononyl) cyclohexane-1,2-dicarboxylate (DINCH) as an alternative plasticizer. Methods: Using a pool-and-split study design, we produced 20 matched homogenous quintets of RBC concentrates in two DINCH bags and three DEHP bags with citrate phosphate dextrose adenine (CPDA-1) anticoagulant. RBC storage quality was assessed weekly for 35 days. Results: On day 35, the median hemolysis levels in the DINCH bags (0.297–0.342%) were marginally higher (p < 0.05) than the DEHP bags (0.204–0.240%). All DINCH bags showed <0.8% hemolysis. RBCs in the DINCH bags showed increased mean corpuscular volume and decreased eosin 5′ maleimide binding than in the DEHP bags. Higher pO2 and lower pCO2 levels in the DINCH bags indicated better gas permeability than in DEHP bags. Other metabolic parameters were comparable in both bags. Compared to DEHP, DINCH exhibited considerably lower levels of plasticizer leaching into blood bags. Conclusion: The quality of RBC concentrates stored for 35 days in DINCH-plasticized blood bags with CDPA-1 is generally comparable to those in DEHP bags. Hence, DINCH can be a viable alternative to DEHP in blood bags for nonleukoreduced RBC storage even without the use of next-generation additive solutions to improve RBC preservation quality.","PeriodicalId":505859,"journal":{"name":"Transfusion Medicine and Hemotherapy","volume":"20 9","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-01-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139387099","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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