Best practice BioBanking of human heart tissue

Lal, Sean; Li, Amy; Allen, D.M.; Allen, Paul D.; Bannon, Paul G.; Cartmill, T.; Cooke, Roger; Farnsworth, Alan; Keogh, Anne; Remedios, Cristobal dos

doi:10.1007/s12551-015-0182-6

Cited by 33 publications

(34 citation statements)

References 24 publications

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“…Tissue MicroArrays (TMAs) are an increasingly common tool for high‐throughput proteomic profiling . Similarly, the advent of tissue biorepositories has seen a rise in the number of genomic and proteomic studies that are being undertaken using cryopreserved human hearts . Here, we describe the construction of human cardiac TMAs consisting of 1 mm diameter cores taken from paraffin‐embedded samples that had previously been cryopreserved and apply this to screen for a target protein of interest—in this case, four‐and‐a‐half LIM‐domain 2 (FHL2).…”

Section: Introductionmentioning

confidence: 99%

Tissue microarray profiling in human heart failure

et al. 2016

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Tissue MicroArrays (TMAs) are a versatile tool for high-throughput protein screening, allowing qualitative analysis of a large number of samples on a single slide. We have developed a customizable TMA system that uniquely utilizes cryopreserved human cardiac samples from both heart failure and donor patients to produce formalin-fixed paraffin-embedded sections. Confirmatory upstream or downstream molecular studies can then be performed on the same (biobanked) cryopreserved tissue. In a pilot study, we applied our TMAs to screen for the expression of four-and-a-half LIM-domain 2 (FHL2), a member of the four-and-a-half LIM family. This protein has been implicated in the pathogenesis of heart failure in a variety of animal models. While FHL2 is abundant in the heart, not much is known about its expression in human heart failure. For this purpose, we generated an affinity-purified rabbit polyclonal anti-human FHL2 antibody. Our TMAs allowed high-throughput profiling of FHL2 protein using qualitative and semiquantitative immunohistochemistry that proved complementary to Western blot analysis. We demonstrated a significant relative reduction in FHL2 protein expression across different forms of human heart failure.

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Section: Introductionmentioning

confidence: 99%

Tissue microarray profiling in human heart failure

et al. 2016

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“…In recent years, the Sydney Heart Bank (SHB) has applied industry best practice to the way it handles banked human tissue (Lal et al 2015). A concise description (~two pages) of the research project is assessed by an independent SHB Board that includes international cardiac researchers, cardiologists, and cardiac surgeons who assess all requests for tissue including those in the SHB.…”

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confidence: 99%

The Sydney Heart Bank: improving translational research while eliminating or reducing the use of animal models of human heart disease

Remedios

Lal

et al. 2017

Biophys Rev

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The Sydney Heart Bank (SHB) is one of the largest human heart tissue banks in existence. Its mission is to provide high-quality human heart tissue for research into the molecular basis of human heart failure by working collaboratively with experts in this field. We argue that, by comparing tissues from failing human hearts with age-matched non-failing healthy donor hearts, the results will be more relevant than research using animal models, particularly if their physiology is very different from humans. Tissue from heart surgery must generally be used soon after collection or it significantly deteriorates. Freezing is an option but it raises concerns that freezing causes substantial damage at the cellular and molecular level. The SHB contains failing samples from heart transplant patients and others who provided informed consent for the use of their tissue for research. All samples are cryopreserved in liquid nitrogen within 40 min of their removal from the patient, and in less than 5-10 min in the case of coronary arteries and left ventricle samples. To date, the SHB has collected tissue from about 450 failing hearts (>15,000 samples) from patients with a wide range of etiologies as well as increasing numbers of cardiomyectomy samples from patients with hypertrophic cardiomyopathy. The Bank also has hearts from over 120 healthy This article is part of a Special Issue on 'IUPAB Edinburgh Congress' edited by Damien Hall.Electronic supplementary material The online version of this article

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“…30 Tissue samples from idiopathic DCM failing hearts were obtained from patients in the age range, 27 to 63 years (5 males, 3 females) or familial DCM 15 to 54 years (8 males) who underwent heart transplantation because of severe systolic dysfunction in New York Heart Association class III or IV. Donors were aged 19 to 65 years (8 males, 7 females) with no history of cardiac dysfunction.…”

Section: Collection Of Human Samplesmentioning

confidence: 99%

Sarcomeric Auto-Oscillations in Single Myofibrils From the Heart of Patients With Dilated Cardiomyopathy

Kagemoto

Oyama

Yamane

et al. 2018

Circ: Heart Failure

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Background: Left ventricular wall motion is depressed in patients with dilated cardiomyopathy (DCM). However, whether or not the depressed left ventricular wall motion is caused by impairment of sarcomere dynamics remains to be fully clarified. Methods and Results: We analyzed the mechanical properties of single sarcomere dynamics during sarcomeric auto-oscillations (calcium spontaneous oscillatory contractions [Ca-SPOC]) that occurred at partial activation under the isometric condition in myofibrils from donor hearts and from patients with severe DCM (New York Heart Association classification III-IV). Ca-SPOC reproducibly occurred in the presence of 1 μmol/L free Ca 2+ in both nonfailing and DCM myofibrils, and sarcomeres exhibited a saw-tooth waveform along single myofibrils composed of quick lengthening and slow shortening. The period of Ca-SPOC was longer in DCM myofibrils than in nonfailing myofibrils, in association with prolonged shortening time. Lengthening time was similar in both groups. Then, we performed Tn (troponin) exchange in myofibrils with a DCM-causing homozygous mutation (K36Q) in cTnI (cardiac TnI). On exchange with the Tn complex from healthy porcine ventricles, period, shortening time, and shortening velocity in cTnI-K36Q myofibrils became similar to those in Tn-reconstituted nonfailing myofibrils. Protein kinase A abbreviated period in both Tn-reconstituted nonfailing and cTnI-K36Q myofibrils, demonstrating acceleration of cross-bridge kinetics. Conclusions: Sarcomere dynamics was found to be depressed under loaded conditions in DCM myofibrils because of impairment of thick-thin filament sliding. Thus, microscopic analysis of Ca-SPOC in human cardiac myofibrils is beneficial to systematically unveil the kinetic properties of single sarcomeres in various types of heart disease.

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Best practice BioBanking of human heart tissue

Cited by 33 publications

References 24 publications

Tissue microarray profiling in human heart failure

Tissue microarray profiling in human heart failure

The Sydney Heart Bank: improving translational research while eliminating or reducing the use of animal models of human heart disease

Sarcomeric Auto-Oscillations in Single Myofibrils From the Heart of Patients With Dilated Cardiomyopathy

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