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Article ; Online: Psychometric Evaluation of the Misophonia Impact Questionnaire (MIQ) Using a Clinical Population of Patients Seeking Help for Tinnitus, Hyperacusis and/or Misophonia.

Aazh, Hashir / Moore, Brian C J / Scaglione, Tricia / Remmert, Nico

Journal of the American Academy of Audiology

2023

Abstract: Background: Misophonia is a decreased tolerance of certain sounds related to eating noises, lip smacking, sniffing, breathing, clicking sounds, and tapping. While several validated self-report misophonia questionnaires exist, none focus solely on the ... ...

Abstract	Background: Misophonia is a decreased tolerance of certain sounds related to eating noises, lip smacking, sniffing, breathing, clicking sounds, and tapping. While several validated self-report misophonia questionnaires exist, none focus solely on the impact of misophonia on the patient's life. Additionally, there are no available validated pediatric self-report measures of misophonia. Therefore, a tool was needed to assess the impact of misophonia on both adult and pediatric patients. Purpose: To evaluate the psychometric properties of the 8-item Misophonia Impact Questionnaire (MIQ). Research design: This was a retrospective cross-sectional study. Study sample: Patients who attended the Tinnitus and Hyperacusis Therapy Specialist Clinic (THTSC) in the UK seeking help for tinnitus, hyperacusis and/or misophonia (n = 256). A subsample of children aged 16 years or younger (n=15) was included for preliminary analyses of a version of the MIQ to be filled in by a parent (MIQ-P). Data collection and analysis: Data were collected retrospectively from the records of patients held at the audiology department. These included demographic data, audiological measures and self-report questionnaires taken as part of routine care. Descriptive statistics and psychometric analyses were conducted. The MIQ was analyzed for item difficulty, factor structure, reliability, and construct validity. Results: Confirmatory factor analysis revealed that a one-factor model for the MIQ gave an excellent fit and its estimated reliability was excellent, with Cronbach's α = 0.94. The total MIQ scores were highly correlated with scores for the Hyperacusis Impact Questionnaire (HIQ) and Sound Sensitivity Symptoms Questionnaire (SSSQ). MIQ scores were not significantly correlated with scores for the Tinnitus Impact Questionnaire (TIQ) or average hearing thresholds. Preliminary data from the sub-sample indicated excellent internal consistency for the MIQ-P, with Cronbach's α = 0.92. Conclusions: The MIQ is a promising questionnaire for assessing the impact of misophonia. Future studies should focus on establishing test/re-test reliability, identifying clinically significant change in MIQ scores, defining the severity of misophonia impact categories, and further exploring the psychometric properties of the MIQ-P.
Language	English
Publishing date	2023-10-16
Publishing country	United States
Document type	Journal Article
ZDB-ID	1132599-9
ISSN	2157-3107 ; 1050-0545
ISSN (online)	2157-3107
ISSN	1050-0545
DOI	10.1055/a-2192-5668
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Article: Psychometric Evaluation of the Misophonia Impact Questionnaire (MIQ) Using a Clinical Population of Patients Seeking Help for Tinnitus, Hyperacusis and/or Misophonia

Aazh, Hashir / Moore, Brian C.J. / Scaglione, Tricia / Remmert, Nico

Journal of the American Academy of Audiology

2023

Abstract	Background: Misophonia is a decreased tolerance of certain sounds related to eating noises, lip smacking, sniffing, breathing, clicking sounds, and tapping. While several validated self-report misophonia questionnaires exist, none focus solely on the impact of misophonia on the patient’s life. Additionally, there are no available validated pediatric self-report measures of misophonia. Therefore, a tool was needed to assess the impact of misophonia on both adult and pediatric patients. Purpose: To evaluate the psychometric properties of the 8-item Misophonia Impact Questionnaire (MIQ). Research Design: This was a retrospective cross-sectional study. Study Sample: Patients who attended the Tinnitus and Hyperacusis Therapy Specialist Clinic (THTSC) in the UK seeking help for tinnitus, hyperacusis and/or misophonia (n = 256). A subsample of children aged 16 years or younger (n=15) was included for preliminary analyses of a version of the MIQ to be filled in by a parent (MIQ-P). Data Collection and Analysis: Data were collected retrospectively from the records of patients held at the audiology department. These included demographic data, audiological measures and self-report questionnaires taken as part of routine care. Descriptive statistics and psychometric analyses were conducted. The MIQ was analyzed for item difficulty, factor structure, reliability, and construct validity. Results: Confirmatory factor analysis revealed that a one-factor model for the MIQ gave an excellent fit and its estimated reliability was excellent, with Cronbach’s α = 0.94. The total MIQ scores were highly correlated with scores for the Hyperacusis Impact Questionnaire (HIQ) and Sound Sensitivity Symptoms Questionnaire (SSSQ). MIQ scores were not significantly correlated with scores for the Tinnitus Impact Questionnaire (TIQ) or average hearing thresholds. Preliminary data from the sub-sample indicated excellent internal consistency for the MIQ-P, with Cronbach’s α = 0.92. Conclusions: The MIQ is a promising questionnaire for assessing the impact of misophonia. Future studies should focus on establishing test/re-test reliability, identifying clinically significant change in MIQ scores, defining the severity of misophonia impact categories, and further exploring the psychometric properties of the MIQ-P.
Language	English
Publishing date	2023-10-16
Publisher	Thieme Medical Publishers, Inc.
Publishing place	Stuttgart ; New York
Document type	Article
ZDB-ID	1132599-9
ISSN	2157-3107 ; 1050-0545
ISSN (online)	2157-3107
ISSN	1050-0545
DOI	10.1055/a-2192-5668
Database	Thieme publisher's database

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Article ; Online: Chemical Regulation of the Protein Quality Control E3 Ubiquitin Ligase C-Terminus of Hsc70 Interacting Protein (CHIP).

Kanack, Adam J / Olp, Michael D / Newsom, Oliver J / Scaglione, Jamie B / Gooden, David M / McMahon, Kevin / Smith, Brian C / Scaglione, K Matthew

Chembiochem : a European journal of chemical biology

2022 Volume 23, Issue 6, Page(s) e202100633

Abstract: The ubiquitin ligase C-terminus of Hsc70 interacting protein (CHIP) is an important regulator of proteostasis. Despite playing an important role in maintaining proteostasis, little progress has been made in developing small molecules that regulate ... ...

Abstract	The ubiquitin ligase C-terminus of Hsc70 interacting protein (CHIP) is an important regulator of proteostasis. Despite playing an important role in maintaining proteostasis, little progress has been made in developing small molecules that regulate ubiquitin transfer by CHIP. Here we used differential scanning fluorimetry to identify compounds that bound CHIP. Compounds that bound CHIP were then analyzed by quantitative ubiquitination assays to identify those that altered CHIP function. One compound, MS.001, inhibited both the chaperone binding and ubiquitin ligase activity of CHIP at low micromolar concentrations. Interestingly, we found that MS.001 did not have activity against isolated U-box or tetratricopeptide (TPR) domains, but instead only inhibited full-length CHIP. Using in silico docking we identified a potential MS.001 binding site on the linker domain of CHIP and mutation of this site rendered CHIP resistant to MS.001. Together our data identify an inhibitor of the E3 ligase CHIP and provides insight into the development of compounds that regulate CHIP activity.
MeSH term(s)	Protein C/genetics ; Protein C/metabolism ; Protein Structure, Tertiary ; Ubiquitin/metabolism ; Ubiquitin-Protein Ligases/metabolism ; Ubiquitination
Chemical Substances	Protein C ; Ubiquitin ; Ubiquitin-Protein Ligases (EC 2.3.2.27)
Language	English
Publishing date	2022-02-03
Publishing country	Germany
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
ZDB-ID	2020469-3
ISSN	1439-7633 ; 1439-4227
ISSN (online)	1439-7633
ISSN	1439-4227
DOI	10.1002/cbic.202100633
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Article ; Online: Single-cell NAD(H) levels predict clonal lymphocyte expansion dynamics.

Science immunology

2024 Volume 9, Issue 93, Page(s) eadj7238

Abstract: Adaptive immunity requires the expansion of high-affinity lymphocytes from a heterogeneous pool. Whereas current models explain this through signal transduction, we hypothesized that antigen affinity tunes discrete metabolic pathways to license clonal ... ...

Abstract	Adaptive immunity requires the expansion of high-affinity lymphocytes from a heterogeneous pool. Whereas current models explain this through signal transduction, we hypothesized that antigen affinity tunes discrete metabolic pathways to license clonal lymphocyte dynamics. Here, we identify nicotinamide adenine dinucleotide (NAD) biosynthesis as a biochemical hub for the T cell receptor affinity-dependent metabolome. Through this central anabolic role, we found that NAD biosynthesis governs a quiescence exit checkpoint, thereby pacing proliferation. Normalizing cellular NAD(H) likewise normalizes proliferation across affinities, and enhancing NAD biosynthesis permits the expansion of lower affinity clones. Furthermore, single-cell differences in NAD(H) could predict division potential for both T and B cells, before the first division, unmixing proliferative heterogeneity. We believe that this supports a broader paradigm in which complex signaling networks converge on metabolic pathways to control single-cell behavior.
MeSH term(s)	NAD ; Lymphocytes/metabolism ; Metabolome ; Signal Transduction
Chemical Substances	NAD (0U46U6E8UK)
Language	English
Publishing date	2024-03-15
Publishing country	United States
Document type	Journal Article
ISSN	2470-9468
ISSN (online)	2470-9468
DOI	10.1126/sciimmunol.adj7238
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Article ; Online: SRCP1 Conveys Resistance to Polyglutamine Aggregation.

Santarriaga, Stephanie / Haver, Holly N / Kanack, Adam J / Fikejs, Alicia S / Sison, Samantha L / Egner, John M / Bostrom, Jonathan R / Seminary, Emily R / Hill, R Blake / Link, Brian A / Ebert, Allison D / Scaglione, K Matthew

Molecular cell

2018 Volume 71, Issue 2, Page(s) 216–228.e7

Abstract: The polyglutamine (polyQ) diseases are a group of nine neurodegenerative diseases caused by the expansion of a polyQ tract that results in protein aggregation. Unlike other model organisms, Dictyostelium discoideum is a proteostatic outlier, naturally ... ...

Abstract	The polyglutamine (polyQ) diseases are a group of nine neurodegenerative diseases caused by the expansion of a polyQ tract that results in protein aggregation. Unlike other model organisms, Dictyostelium discoideum is a proteostatic outlier, naturally encoding long polyQ tracts yet resistant to polyQ aggregation. Here we identify serine-rich chaperone protein 1 (SRCP1) as a molecular chaperone that is necessary and sufficient to suppress polyQ aggregation. SRCP1 inhibits aggregation of polyQ-expanded proteins, allowing for their degradation via the proteasome, where SRCP1 is also degraded. SRCP1's C-terminal domain is essential for its activity in cells, and peptides that mimic this domain suppress polyQ aggregation in vitro. Together our results identify a novel type of molecular chaperone and reveal how nature has dealt with the problem of polyQ aggregation.
MeSH term(s)	Cell Line ; Dictyostelium/metabolism ; HEK293 Cells ; Humans ; Molecular Chaperones/metabolism ; Peptides/metabolism ; Proteasome Endopeptidase Complex/metabolism ; Protein Binding ; Serine/metabolism ; Ubiquitin/metabolism
Chemical Substances	Molecular Chaperones ; Peptides ; Ubiquitin ; polyglutamine (26700-71-0) ; Serine (452VLY9402) ; Proteasome Endopeptidase Complex (EC 3.4.25.1)
Language	English
Publishing date	2018-07-19
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	1415236-8
ISSN	1097-4164 ; 1097-2765
ISSN (online)	1097-4164
ISSN	1097-2765
DOI	10.1016/j.molcel.2018.07.008
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Zs.A 5055: Show issues

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Article: SRCP1 Conveys Resistance to Polyglutamine Aggregation

Santarriaga, Stephanie / Haver, Holly N / Kanack, Adam J / Fikejs, Alicia S / Sison, Samantha L / Egner, John M / Bostrom, Jonathan R / Seminary, Emily R / Hill, R. Blake / Link, Brian A / Ebert, Allison D / Scaglione, K. Matthew

Molecular cell. 2018 July 19, v. 71, no. 2

2018

Abstract	The polyglutamine (polyQ) diseases are a group of nine neurodegenerative diseases caused by the expansion of a polyQ tract that results in protein aggregation. Unlike other model organisms, Dictyostelium discoideum is a proteostatic outlier, naturally encoding long polyQ tracts yet resistant to polyQ aggregation. Here we identify serine-rich chaperone protein 1 (SRCP1) as a molecular chaperone that is necessary and sufficient to suppress polyQ aggregation. SRCP1 inhibits aggregation of polyQ-expanded proteins, allowing for their degradation via the proteasome, where SRCP1 is also degraded. SRCP1’s C-terminal domain is essential for its activity in cells, and peptides that mimic this domain suppress polyQ aggregation in vitro. Together our results identify a novel type of molecular chaperone and reveal how nature has dealt with the problem of polyQ aggregation.
Keywords	Dictyostelium discoideum ; amino acid sequences ; models ; molecular chaperones ; neurodegenerative diseases ; peptides ; proteasome endopeptidase complex
Language	English
Dates of publication	2018-0719
Size	p. 216-228.e7.
Publishing place	Elsevier Inc.
Document type	Article
ZDB-ID	1415236-8
ISSN	1097-4164 ; 1097-2765
ISSN (online)	1097-4164
ISSN	1097-2765
DOI	10.1016/j.molcel.2018.07.008
Database	NAL-Catalogue (AGRICOLA)

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Article ; Online: Correcting miR-15a/16 genetic defect in New Zealand Black mouse model of CLL enhances drug sensitivity.

Salerno, Erica / Scaglione, Brian J / Coffman, Frederick D / Brown, Brian D / Baccarini, Alessia / Fernandes, Helen / Marti, Gerald / Raveche, Elizabeth S

Molecular cancer therapeutics

2009 Volume 8, Issue 9, Page(s) 2684–2692

Abstract: Alterations in the human 13q14 genomic region containing microRNAs mir-15a and mir-16-1 are present in most human chronic lymphocytic leukemia (CLL). We have previously found the development of CLL in the New Zealand Black murine model to be associated ... ...

Abstract	Alterations in the human 13q14 genomic region containing microRNAs mir-15a and mir-16-1 are present in most human chronic lymphocytic leukemia (CLL). We have previously found the development of CLL in the New Zealand Black murine model to be associated with a point mutation in the primary mir-15a/16-1 region, which correlated with a decrease in mature miR-16 and miR-15a levels. In this study, addition of exogenous miR-15a and miR-16 led to an accumulation of cells in G(1) in non-New Zealand Black B cell and New Zealand Black-derived malignant B-1 cell lines. However, the New Zealand Black line had significantly greater G(1) accumulation, suggesting a restoration of cell cycle control upon exogenous miR-15a/16 addition. Our experiments showed a reduction in protein levels of cyclin D1, a miR-15a/16 target and cell cycle regulator of G(1)/S transition, in the New Zealand Black cell line following miR-15a/16 addition. These microRNAs were shown to directly target the cyclin D1 3' untranslated region using a green fluorescent protein lentiviral expression system. miR-16 was also shown to augment apoptosis induction by nutlin, a mouse double minute 2 (MDM2) antagonist, and genistein, a tyrosine kinase inhibitor, when added to a B-1 cell line derived from multiple in vivo passages of malignant B-1 cells from New Zealand Black mice with CLL. miR-16 synergized with nutlin and genistein to induce apoptosis. Our data support a role for the mir-15a/16-1 cluster in cell cycle regulation and suggest that these mature microRNAs in both the New Zealand Black model and human CLL may be targets for therapeutic efficacy in this disease.
MeSH term(s)	Animals ; Antineoplastic Agents/pharmacology ; Apoptosis ; Base Sequence ; Cyclin D1/genetics ; DNA Primers ; Disease Models, Animal ; Drug Screening Assays, Antitumor ; Genistein/therapeutic use ; Imidazoles/therapeutic use ; Leukemia, Lymphocytic, Chronic, B-Cell/drug therapy ; Leukemia, Lymphocytic, Chronic, B-Cell/genetics ; Leukemia, Lymphocytic, Chronic, B-Cell/pathology ; Mice ; Mice, Inbred C57BL ; MicroRNAs/genetics ; Piperazines/therapeutic use ; RNA, Messenger/genetics
Chemical Substances	Antineoplastic Agents ; DNA Primers ; Imidazoles ; MicroRNAs ; Piperazines ; RNA, Messenger ; Cyclin D1 (136601-57-5) ; nutlin 3 (53IA0V845C) ; Genistein (DH2M523P0H)
Language	English
Publishing date	2009-09-01
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2063563-1
ISSN	1538-8514 ; 1535-7163
ISSN (online)	1538-8514
ISSN	1535-7163
DOI	10.1158/1535-7163.MCT-09-0127
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Article ; Online: Mutation of the IFNAR-1 receptor binding site of human IFN-alpha2 generates type I IFN competitive antagonists.

Pan, Manjing / Kalie, Eyal / Scaglione, Brian J / Raveche, Elizabeth S / Schreiber, Gideon / Langer, Jerome A

Biochemistry

2008 Volume 47, Issue 46, Page(s) 12018–12027

Abstract: Type I interferons (IFNs) are multifunctional cytokines that activate cellular responses by binding a common receptor consisting of two subunits, IFNAR-1 and IFNAR-2. Although the binding of IFNs to IFNAR-2 is well characterized, the binding to the lower ...

Abstract	Type I interferons (IFNs) are multifunctional cytokines that activate cellular responses by binding a common receptor consisting of two subunits, IFNAR-1 and IFNAR-2. Although the binding of IFNs to IFNAR-2 is well characterized, the binding to the lower affinity IFNAR-1 remains less well understood. Previous reports identified a region of human IFN-alpha2 on the B and C helices ("site 1A": N65, L80, Y85, Y89) that plays a key role in binding IFNAR-1 and contributes strongly to differential activation by various type I IFNs. The current studies demonstrate that residues on the D helix are also involved in IFNAR-1 binding. In particular, residue 120 (Arg in IFN-alpha2; Lys in IFN-alpha2/alpha1) appears to be a "hot-spot" residue: substitution by alanine significantly decreased biological activity, and the charge-reversal mutation of residue 120 to Glu caused drastic loss of antiviral and antiproliferative activity for both IFN-alpha2 and IFN-alpha2/alpha1. Mutations in residues of helix D maintained their affinity for IFNAR-2 but had decreased affinity for IFNAR-1. Single-site or multiple-site mutants in the IFNAR-1 binding site that had little or no detectable in vitro biological activity were capable of blocking in vitro antiviral and antiproliferative activity of native IFN-alpha2; i.e., they are type I IFN antagonists. These prototype IFN antagonists can be developed further for possible therapeutic use in systemic lupus erythematosus, and analogous molecules can be designed for use in animal models.
MeSH term(s)	Amino Acid Substitution ; Animals ; Binding Sites/genetics ; Cattle ; Disease Models, Animal ; Humans ; Interferon-alpha/antagonists & inhibitors ; Interferon-alpha/chemistry ; Interferon-alpha/genetics ; Interferon-alpha/metabolism ; Lupus Erythematosus, Systemic/drug therapy ; Lupus Erythematosus, Systemic/genetics ; Lupus Erythematosus, Systemic/metabolism ; Mice ; Protein Binding/genetics ; Protein Structure, Secondary/genetics ; Receptor, Interferon alpha-beta/chemistry ; Receptor, Interferon alpha-beta/genetics ; Receptor, Interferon alpha-beta/metabolism
Chemical Substances	IFNAR1 protein, human ; IFNAR2 protein, human ; Ifnar1 protein, mouse ; Ifnar2 protein, mouse ; Interferon-alpha ; Receptor, Interferon alpha-beta (156986-95-7)
Language	English
Publishing date	2008-11-18
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1108-3
ISSN	1520-4995 ; 0006-2960
ISSN (online)	1520-4995
ISSN	0006-2960
DOI	10.1021/bi801588g
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Article ; Online: Murine models of chronic lymphocytic leukaemia: role of microRNA-16 in the New Zealand Black mouse model.

Scaglione, Brian J / Salerno, Erica / Balan, Murugabaskar / Coffman, Frederick / Landgraf, Pablo / Abbasi, Fatima / Kotenko, Sergei / Marti, Gerald E / Raveche, Elizabeth S

British journal of haematology

2007 Volume 139, Issue 5, Page(s) 645–657

Abstract: Mouse models are valuable tools in the study of human chronic lymphocytic leukaemia (CLL). The New Zealand Black (NZB) strain is a naturally occurring model of late-onset CLL characterized by B-cell hyperproliferation and autoimmunity early in life, ... ...

Abstract	Mouse models are valuable tools in the study of human chronic lymphocytic leukaemia (CLL). The New Zealand Black (NZB) strain is a naturally occurring model of late-onset CLL characterized by B-cell hyperproliferation and autoimmunity early in life, followed by progression to CLL. Other genetically engineered models of CLL that have been developed include (NZB x NZW) F1 mice engineered to express IL5, mice expressing human TCL1A, and mice overexpressing both BCL2 and a tumour necrosis factor receptor-associated factor. The applicability to human CLL varies with each model, suggesting that CLL is a multifactorial disease. Our work with the de novo NZB model has revealed many similarities to the human situation, particularly familial CLL. In NZB, the malignant clones express CD5, zap-70, and have chromosomal instability and germline Ig sequence. We also identified a point mutation in the 3'-flanking sequence of Mirn16-1, which resulted in decreased levels of the microRNA, miR-16 in lymphoid tissue. Exogenous restoration of miR-16 to an NZB malignant B-1 cell line resulted in cell cycle alterations, suggesting that the altered expression of Mirn15a/16-1 is an important molecular lesion in CLL. Future studies utilizing the NZB mouse could ascertain the role of environmental triggers, such as low dose radiation and organic chemicals in the augmentation of a pre-existing propensity to develop CLL.
MeSH term(s)	Animals ; Base Sequence ; Disease Models, Animal ; Leukemia, Lymphocytic, Chronic, B-Cell/genetics ; Mice ; Mice, Inbred NZB ; Mice, Transgenic ; MicroRNAs/genetics ; Molecular Sequence Data ; Point Mutation ; RNA, Neoplasm/genetics
Chemical Substances	MicroRNAs ; RNA, Neoplasm
Language	English
Publishing date	2007-10-17
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	80077-6
ISSN	1365-2141 ; 0007-1048
ISSN (online)	1365-2141
ISSN	0007-1048
DOI	10.1111/j.1365-2141.2007.06851.x
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Article ; Online: The New Zealand black mouse as a model for the development and progression of chronic lymphocytic leukemia.

Salerno, Erica / Yuan, Yao / Scaglione, Brian J / Marti, Gerald / Jankovic, Alexander / Mazzella, Fermina / Laurindo, Maria Fernanda / Despres, Daryl / Baskar, Sivasubramanian / Rader, Christoph / Raveche, Elizabeth

Cytometry. Part B, Clinical cytometry

2010 Volume 78 Suppl 1, Page(s) S98–109

Abstract: Background: Similar to a subset of human patients who progress from monoclonal B lymphocytosis (MBL) to chronic lymphocytic leukemia (CLL), New Zealand Black (NZB) mice have an age-associated progression to CLL. The murine disease is linked to a genetic ...

Abstract	Background: Similar to a subset of human patients who progress from monoclonal B lymphocytosis (MBL) to chronic lymphocytic leukemia (CLL), New Zealand Black (NZB) mice have an age-associated progression to CLL. The murine disease is linked to a genetic abnormality in microRNA mir-15a/16-1 locus, resulting in decreased mature miR-15a/16. Methods: Spleens of aging NZB were analyzed for the presence of B-1 cells via flow cytometry and for the presence of a side population (SP) via the ability of cells to exclude Hoechst 33342 dye. The SP was assayed for the presence of hyperdiploid B-1 clones and for the ability to differentiate into B-1 cells in vitro and transfer disease in vivo. In addition, enhanced apoptosis of chemoresistant NZB B-1 cells was examined by restoring miR-16 levels in nutlin-treated cells. Results: Aging NZB mice develop a B-1 expansion and clonal development that evolves from MBL into CLL. An expansion in SP is also seen. Although the SP did contain increased cells with stem cell markers, they lacked malignant B-1 cells and did not transfer disease in vivo. Similar to B-1 cells, splenic NZB SP also has decreased miR-15a/16 when compared with C57Bl/6. Exogenous addition of miR-15a/16 to NZB B-1 cells resulted in increased sensitivity to nutlin. Conclusion: NZB serve as an excellent model for studying the development and progression of age-associated CLL. NZB SP cells do not seem to contain cancer stem cells, but rather the B-1 stem cell. NZB B-1 chemoresistance may be related to reduced miR-15a/16 expression.
MeSH term(s)	Age Factors ; Animals ; Apoptosis/drug effects ; Cell Separation ; Cell Survival ; Disease Models, Animal ; Disease Progression ; Female ; Flow Cytometry ; Imidazoles/pharmacology ; Immunophenotyping ; Leukemia, Lymphocytic, Chronic, B-Cell/immunology ; Leukemia, Lymphocytic, Chronic, B-Cell/pathology ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Inbred NZB ; Piperazines/pharmacology ; Spleen/drug effects ; Spleen/immunology ; Spleen/pathology
Chemical Substances	Imidazoles ; Piperazines ; nutlin 1
Language	English
Publishing date	2010-09-13
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2099657-3
ISSN	1552-4957 ; 1552-4949 ; 0196-4763
ISSN (online)	1552-4957
ISSN	1552-4949 ; 0196-4763
DOI	10.1002/cyto.b.20544
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