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How much Cardiomyocyte Move in Relation to its Neurons?

How much Cardiomyocyte Move in Relation to its Neurons?


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I am trying to estimate how much cardiomyocyte and its things (mitochondria) move in relation to neurons

  1. Movement of neurons (1)
  2. Movement of cardiomyocytes
  3. Movement of cardiomyocytes' mitochondrias (2)
  4. Movement of stem cells - I think we can ignore this one

Motivation: some imaging projects have focused on the neurons etc ECG/… because they move relatively little in comparison to cardiomyocytes and their organelles; my interest is in the electromuscular view and I would like to understand how the movement of cardiomyocytes and their mitochondrias could be adjusted/calibrated in the time-frequency (t-f) data (spectrogram/… ) of cardiomyocytes

Pseudocode

Simplistic view about including the effect of cytoarchitecture of organelles on the dynamics/movements based on statistics and probabilistic approaches

function getMitochondriaDynamics2D(signal2D, edges, Cytoarchitecture): signal2D=$1; edgesN=size($2,2); organelles=[neurons, cardiomyocyte_minus_mitochondia, mitochondria,… ]; % given organelles.cytoarchitecture = $3; % probabilistic values in Statistics organelles.dynamics = zeros(1,edgesN-1); % preallocation % Limit dynamics by cytoarchitectural restrictions for organelle in organelles % include here systemic effects on organelles but Ignored here % etc Age, Smoking,… % Let's loop local changes for edge in organelles.dynamics organelle.dynamics(edge) = organelle.dynamics(edge) .*… organelle.cytoarchitecture(edge); end end return signal2D .*organelle(mitochondria).dynamics; end %% TODO here function analysisMitochondriaDynamics2D(dynamics2D)… end

To find those probabilistic values

  • Embryology but I am weak here
  • databases and/or publications - which?

Biochemistry

I do not understand how much this should be considered here, but it could help to get any model

  • Atrial cardiomyocyte calcium signalling
  • mobility of the delayed-rectifer K+ channel Kv2.1 (3)

Useful keywoards

  • cardiomyocyte adult mobility

Hypothesis and Math/Physics/Bio

Hypothetical View of t-f data (2D) in cardiomyocytes: regular points separated by steady-gel-like areas - - seems to artifact of the movement

Physics about characterizing such areas:

  • … [ which mathematical methods ]…

Sources

There are much studies in Embryology about cardiomyocytes and their movement, but I cannot understand their relation in the topic

  1. Piquereau, Mitochondrial dynamics in the adult cardiomyocytes: which roles for a highly specialized cell?, 2013
  2. How to measure Na/K channel activation at the membrane level?
  3. Localization and mobility of the delayed-rectifer K+ channel Kv2.1 in adult cardiomyocytes.
  4. Mitochondrial dynamics in the adult cardiomyocytes: which roles for a highly specialized cell?
  5. PubMed withcardiomyocyte+"patch clamp", about measuring plated cells which are from hearts freshly minced in collagenase / EDTA. See PMIDs 27364017, 27076034, 26142302, 26241168, 26378152,… [NickSandor]

Useful keywords

  • adult cardiomyocyte
  • possibly: Atrial cardiomyocyte calcium signalling
  • Mitochondrial dynamics
  • cytoarchitecture restrictions dynamics

Proprioception

Proprioception ( / ˌ p r oʊ p r i oʊ ˈ s ɛ p ʃ ən , - p r i ə -/ [1] [2] PROH -pree-o- SEP -shən), also referred to as kinaesthesia (or kinesthesia), is the sense of self-movement and body position. [3] It is sometimes described as the "sixth sense". [4]

Proprioception is mediated by proprioceptors, mechanosensory neurons located within muscles, tendons, and joints. [3] There are multiple types of proprioceptors which are activated during distinct behaviors and encode distinct types of information: limb velocity and movement, load on a limb, and limb limits. Vertebrates and invertebrates have distinct but similar modes of encoding this information.

The central nervous system integrates proprioception and other sensory systems, such as vision and the vestibular system, to create an overall representation of body position, movement, and acceleration.

More recently proprioception has also been described in flowering land plants (angiosperms). [5] [6]


Abstract

Ca 2+ signaling is of vital importance to cardiac cell function and plays an important role in heart failure. It is based on sarcolemmal, sarcoplasmic reticulum and mitochondrial Ca 2+ cycling. While the first two are well characterized, the latter remains unclear, controversial and technically challenging.

In mammalian cardiac myocytes, Ca 2+ influx through L-type calcium channels in the sarcolemmal membrane triggers Ca 2+ release from the nearby junctional sarcoplasmic reticulum to produce Ca 2+ sparks. When this triggering is synchronized by the cardiac action potential, a global [Ca 2+ ]i transient arises from coordinated Ca 2+ release events. The ends of intermyofibrillar mitochondria are located within 20 nm of the junctional sarcoplasmic reticulum and thereby experience a high local [Ca 2+ ] during the Ca 2+ release process. Both local and global Ca 2+ signals may thus influence calcium signaling in mitochondria and, reciprocally, mitochondria may contribute to the local control of calcium signaling. In addition to the intermyofibrillar mitochondria, morphologically distinct mitochondria are also located in the perinuclear and subsarcolemmal regions of the cardiomyocyte and thus experience a different local [Ca 2+ ].

Here we review the literature in regard to several issues of broad interest: (1) the ultrastructural basis for mitochondrion – sarcoplasmic reticulum cross-signaling (2) mechanisms of sarcoplasmic reticulum signaling (3) mitochondrial calcium signaling and (4) the possible interplay of calcium signaling between the sarcoplasmic reticulum and adjacent mitochondria.

Finally, this review discusses experimental findings and mathematical models of cardiac calcium signaling between the sarcoplasmic reticulum and mitochondria, identifies weaknesses in these models, and suggests strategies and approaches for future investigations.


Cardiac specification and development

The formation of the mammalian heart is regulated by the interplay between major developmental signaling pathways, an increasingly cardiac-specific array of transcription factors, as well as other transcriptional regulators. The four-chambered heart consists of the left and right atria, left and right ventricles (the myocardial components), the epicardium (the outer epithelial layer of the heart) and the endocardium (inner endothelial layer of the heart) (Fig. 1). The major cell types of the heart include cardiomyocytes, cardiac conduction cells, cardiac fibroblasts and vascular smooth muscle cells (predominantly within the myocardium) and endothelial cells (predominantly within the myocardium and endocardium) (Fig. 2). The cardiomyocyte lineage is highly specialized, consisting of several different subtypes defined both by their location and function (see Box 2). The first step in understanding how to generate functional and mature cardiomyocytes in vitro is to unravel the complexity that is intrinsic to their formation in vivo.

Cardiac development in the mouse embryo. Following gastrulation, the cells of the inner cell mass (ICM) are specified into three distinct germ layers: endoderm, ectoderm and mesoderm. The first signs of cardiac development can be detected at ∼E6.5 with the formation of the cardiac mesoderm (CM, yellow) at the posterior side of the embryo, along the primitive streak (PS). At E7, the cardiac mesodermal cells migrate towards the anterior side of the embryo to form the two major cardiac progenitor pools: the first heart field (FHF, orange) or cardiac crescent and the second heart field (SHF, blue), located posterior to the crescent. The FHF gives rise to the beating primitive heart tube (PHT) and eventually to the left ventricle (LV) and parts of the right and left atria (RA and LA, respectively). The SHF progenitors, located behind the PHT within the pharyngeal mesoderm (PM, light blue) by E8, migrate towards the primitive and looping heart tube to contribute to the right ventricle (RV), parts of the atria and outflow tract (OFT), and later to the base of the aorta (AO) and pulmonary trunk (PT). At ∼E9.0 the transient proepicardial organ (PEO, purple), which eventually will form the outer lining of the heart known as the epicardium (EPC), becomes apparent. In addition, cardiac neural crest cells (CNCCs, green) migrate in from the dorsal neural tube through the pharyngeal arches, contributing to smooth muscle cells within the aortic and pulmonary arteries. Cells of the venous poles (VP, red), apparent at E8, contribute to the base of the superior and inferior vena cava (SVC and IVC, respectively). ML, midline.

Cardiac development in the mouse embryo. Following gastrulation, the cells of the inner cell mass (ICM) are specified into three distinct germ layers: endoderm, ectoderm and mesoderm. The first signs of cardiac development can be detected at ∼E6.5 with the formation of the cardiac mesoderm (CM, yellow) at the posterior side of the embryo, along the primitive streak (PS). At E7, the cardiac mesodermal cells migrate towards the anterior side of the embryo to form the two major cardiac progenitor pools: the first heart field (FHF, orange) or cardiac crescent and the second heart field (SHF, blue), located posterior to the crescent. The FHF gives rise to the beating primitive heart tube (PHT) and eventually to the left ventricle (LV) and parts of the right and left atria (RA and LA, respectively). The SHF progenitors, located behind the PHT within the pharyngeal mesoderm (PM, light blue) by E8, migrate towards the primitive and looping heart tube to contribute to the right ventricle (RV), parts of the atria and outflow tract (OFT), and later to the base of the aorta (AO) and pulmonary trunk (PT). At ∼E9.0 the transient proepicardial organ (PEO, purple), which eventually will form the outer lining of the heart known as the epicardium (EPC), becomes apparent. In addition, cardiac neural crest cells (CNCCs, green) migrate in from the dorsal neural tube through the pharyngeal arches, contributing to smooth muscle cells within the aortic and pulmonary arteries. Cells of the venous poles (VP, red), apparent at E8, contribute to the base of the superior and inferior vena cava (SVC and IVC, respectively). ML, midline.

Specification and progression of the cardiac cell lineage during development. The stepwise commitment of pluripotent cells via various intermediate stages towards mature cardiac cell types within the heart during development. The intermediate stages can be characterized by specific molecular signatures and the progression of differentiation is influenced by various signaling pathways. EPDCs, epicardium-derived cells EMT, endothelial-to-mesenchymal transition SAN, sinoatrial node RBB, right bundle branch LBB, left bundle branch PF, Purkinje fibers AV, atrioventricular.

Specification and progression of the cardiac cell lineage during development. The stepwise commitment of pluripotent cells via various intermediate stages towards mature cardiac cell types within the heart during development. The intermediate stages can be characterized by specific molecular signatures and the progression of differentiation is influenced by various signaling pathways. EPDCs, epicardium-derived cells EMT, endothelial-to-mesenchymal transition SAN, sinoatrial node RBB, right bundle branch LBB, left bundle branch PF, Purkinje fibers AV, atrioventricular.

Cardiac myocytes of the adult mammalian heart display significant heterogeneity in their function with regard to anatomical location. Specialized cardiac myocyte subtypes include atrial and ventricular cardiomyocytes, and cardiac conduction cells such as those of the sinoatrial node (SAN), the atrioventricular node (AVN), the HIS bundle, the left and right bundle branches (LBB and RBB), and Purkinje fibers. The frequency at which the heart contracts under normal circumstances is determined by the pacemaker cells of the SAN that generate spontaneous action potentials leading to the depolarization and contraction of the atria. The electrical impulses converge on the AVN and spread through the ventricular conduction system (LBB, RBB, Purkinje cells), leading to a depolarization of the syncytium of cardiomyocytes, thereby ensuring orchestrated contraction of the chambers. Nodal, atrial and ventricular cardiomyocytes can be defined based on their location as well as their functional, molecular and electrophysiological properties (see table) the characteristic action potentials (APs) of cardiac myocyte subtypes are illustrated (Atkinson et al., 2011 Bird et al., 2003 Bootman et al., 2011 Chandler et al., 2009 Gourdie et al., 1998 Greener et al., 2011 Hoogaars et al., 2007 Mikawa and Hurtado, 2007 Miquerol et al., 2011 Ng et al., 2010).

Figure 9.1 . In vitro gene delivery using magnectofection.

In in vivo magentofection, the magnetic field is focused over the target site. This method has the potential not only to enhance transfection efficiency but also to target the therapeutic gene to a specific organ or site, as shown in Figure 9.2 .

Figure 9.2 . In vivo gene delivery using magnectofection.

Generally, magnetic particles carrying therapeutic genes are injected intravenously. As the particles flow through the bloodstream, they are captured at the target site using very strong, high-gradient external magnets. Once they are captured, the magnetic particles carrying the therapeutic gene are taken up by the tissue, followed by release of the gene via enzymatic cleavage of cross-linked molecules or degradation of the polymer matrix. If DNA is embedded inside or within the coating material, the magnetic field must be applied to heat the particles and release the gene from the magnetic carrier [ 105 ].


Applications

The ultimate applied goal of regeneration biology is to develop methods to improve regenerative capacity, facilitating disease prevention and recovery. This symposium ran concurrently with the Regenerative Tissue Engineering and Transplantation Symposium, enhancing the diversity of an already well-rounded group of participants. Many talks described the potential or ongoing application of recent discoveries toward therapies.

The application of human embryonic (ES) cells is limited by the availability of only a handful of cell lines. The closing keynote address by Susan Fisher (University of California, San Francisco, USA) described a new method for deriving lines from single, isolated blastomeres. These new lines possess all the properties of existing human ES cell lines, but have many additional characteristics that could make them especially useful for regenerative medicine therapies.

Manipulations that improve regenerative capacity in model systems provide tantalizing glimpses of future possible applications. Ömer Hidir Yilmaz (Massachusetts General Hospital/Whitehead Institute, USA) described how caloric restriction, known to enhance lifespan in many species, improves the capacity for in vitro enteroid formation by intestinal stem cells through a mechanism in which mTORC activity is reduced in Paneth cells (Yilmaz et al., 2012). Gufa Lin (University of Minnesota, USA) showed how a graft of regeneration-competent cells supplemented by a slow-release cocktail of factors, including Shh, Fgf10 and Thymosin Beta-4, could enhance the regeneration of amputated adult Xenopus limbs, which normally would only form a cartilage spike. Eric Lagasse (University of Pittsburgh, USA) is interested in cell therapies that provide function from ectopic sites, and has found promise in lymph nodes (Hoppo et al., 2011). He described how they have been able to transplant hepatocytes, pancreatic beta cell islets, and thymocytes into mouse lymph nodes, where these tissues grow, become vascularized and can serve functions of host organs.

High-throughput model systems give researchers the opportunity to use unbiased approaches to identify compounds and pathways that improve regeneration. Olov Andersson (University of California, San Francisco, USA) combined a system for inducible ablation of β cells in zebrafish larvae with a screen for small molecules that enhance or block the ensuing regeneration. Positive hits revealed that adenosine signaling increased β-cell proliferation and accelerated the restoration of normoglycemia, and these effects were also seen in a diabetic mouse model (Andersson et al., 2012). Finally, Michele de Luca (University of Modena and Reggio Emilia, Italy) presented an inspiring story of successful regenerative medicine, describing the growth and expansion of epithelial stem cells in vitro for skin grafts for severe burn victims. He also showed the long-term success in patients of transplanting corneal epithelium grown from cultured primary limbal stem cells, in which vision was recovered in a high percentage of tissue recipients (Rama et al., 2010). This work demonstrated the desperate need in clinics for regeneration-based discovery research and discovery-driven therapeutic solutions.


Parts of the Nervous System

The center of the nervous system is the brain. The brain takes in what your eyes see and ears hear, and if you decide that you want to move around, your brain tells your muscles to do it.

Your brain makes your muscles move by sending tiny electrical signals to them through your nerves. Remember how neurons can be really long? Well, nerves are just a lot of those really long neurons all bunched together. Those really long neurons each send a small electrical shock to your muscles, which makes them move, moving your body.

The nervous system is really complicated, but it can be divided into two really general parts. One is the Central Nervous System (or CNS). The CNS consists of your brain and spinal cord. The brain and spinal cord are inside your skull and vertebrae (the vertebrae make up your backbone). These bones protect the CNS when you get into accidents.

The other part of the nervous system is the Peripheral Nervous System (or PNS). The PNS consists mainly of the nerves that go to and from the CNS. Unlike the CNS, though, there is no bony protection for the PNS. Have you ever hit your "funny bone?" That odd feeling was you pinching one of the nerves in your arm. That nerve is part of the PNS. It has no bones to protect it so it's easy to hit!


The brain and balls overlap in over 13,000 ways

Riddle me this: Both of these organs guard their contents closely, appear wrinkly on the outside, and can determine the course of an individual life. What are they?

We’re talking about the brain and the testicles.

A review paper published Wednesday in Open Biology makes the case for this curious comparison, laying out the biological similarities between balls and brains. What they have in common, researchers argue, may help us understand conditions that affect both and find better ways to treat them.

“What we brought new to the topic was an exhaustive comparison between brain and testis, taking into account different perspectives,” Margarida Fardilha tells Inverse. Fardilha is the senior author of the review and an assistant professor in the Institute of Biomedicine-iBiMED at the University of Aveiro in Portugal.

Here’s the background — Researchers are finding mounting evidence suggesting brains are more similar to testicles than previously thought.

Previously, it was understood that they shared certain cellular similarities — specialized support cells, for example, called astrocytes in the brain and Sertoli cells in the testes. They both also have boundaries that allow certain materials in and block others out: the blood-brain barrier and the blood-testis barrier.

Brains and testes also, it turns out, have the highest number of genes in common of all the organs.

This could have to do, Fardilha and colleagues explain, with both organ’s roles in distinguishing humans from Earth’s other creatures. This process is called speciation. The large brains we evolved with are, of course, what sets us apart as a species — but the uniqueness of our brain isn’t all that’s different.

“Sperm are the motor for speciation,” the authors write. This because sperm are thought to be a hub for the development of new genes. New genes can hasten the process of evolution because they can encode the instructions for new molecules.

Sperm are also the gatekeepers of the human species, so to speak, making it so we can’t reproduce with other animals. Brain and testes both have outsized roles, the review argues, in ensuring the evolution, and integrity, of humanity.

How they did it — Without knowing about their roles, it might be reasonable to assume that other organs of the body have just as much in common as brains and testes. After all, cells have similar basic structures and the tissues of our body are generally made up of materials that resemble one another.

But the review authors say the brain and testes have more in common on a minute biological level than other parts of the body, writing that the “analysis revealed that, surprisingly, human brain and testes have the highest number of common proteins, compared to other human body tissues.”

Scientists determined this unusual similarity by using a tool called the Human Protein Atlas to identify:

Using another computer program, they then compared them to all the proteins created by 28 other human tissues of the body. The goal was to see where the proteins overlapped.

They did the same thing using slightly different references for sperm cells and neurons, the primary cells of the brain.

Proteins are helpful when identifying and classifying different parts of the body because they are the products of DNA and RNA and can break down into and interact with other chemicals responsible for controlling how the body responds to its environment. The proteins that a certain cell or even a group of cells (a tissue like the heart or lungs) creates distinguishes it from others.

What was discovered — The researchers found in their comparison between the brain and testes that the two were unusually similar, more than the 28 other tissues of the body they evaluated. The brain and testes have 13,442 proteins in common, out of the 14,315 and 15,687 they each create.

In their zoomed-in comparison of the primary cells associated with the brain and testes, the review team found that sperm and neurons also overlapped significantly, if not as dramatically. Of the 6,653 proteins that a sperm cell creates, a neuron also makes 5,048 of them. (Overall, a neuron creates over 13,000 proteins.)

The researchers then looked more closely at the proteins that were the most “highly expressed,” in these tissues and what processes they were related to. While it’s known the brain sends many of the signals that allow sperm to develop in the testes, more recently scientists have found that many of the proteins share roles that are related to brain development — and only a small percentage with sperm development.

The proteins that neurons and sperm shared, for their part, both had to do largely with cell and tissue development, as well as a process called exocytosis. This is when a cell expels materials transported in membrane-wrapped packages into the environment around it.

The overlapping proteins were also involved in cell signaling, a term that describes how cells communicate with one another.

Why it matters — This striking resemblance between the upper and lower packages, the review authors reasoned, had to have a purpose. If they had similar biological functions, maybe it could explain links between conditions that harm both.

As it turns out, there is overlap in a few disorders that affect both brain and testes. For example, multiple sclerosis and male infertility can overlap. Meanwhile, certain dysfunctions of the brain have been linked to changed testicles. Pelvic surgery, diabetes, spinal abnormalities, and spinal cord injury can also lead to male infertility, through erectile dysfunction or semen abnormalities.

Also, and perhaps more controversially, in 2009 scientists found a correlation (which doesn’t mean that one caused the other) between overall intelligence and measures of sperm, like count, concentration, and movement. They reasoned that what makes humans biologically “fit” in one area could also go hand in hand with another. In another study from 2013, researchers actually found a relationship between testes size and parenting behavior: bigger testes sizes were correlated with less nurturing-related brain activity in fathers.

What’s next— If testicles and brains have so much in common, acknowledging and analyzing their shared biology could help move forward treatments for these issues. Or, if there was a treatment that worked for one ailment, it could help guide scientific inquiry in treating the other.

This team argues for a more thorough analysis of the shared proteins and their functions, which they say could lead to a better understanding of the mechanisms underlying diseases and better treatments. And that’s something to go nuts for.


Author information

Affiliations

Department of Pathology,, Institute for Stem Cell Biology and Regenerative Medicine

Thomas Vierbuchen, Austin Ostermeier, Yuko Kokubu & Marius Wernig

Program in Cancer Biology,

Thomas Vierbuchen, Austin Ostermeier & Marius Wernig

Department of Molecular and Cellular Physiology,

Zhiping P. Pang & Thomas C. Südhof

Howard Hughes Medical Institute, Stanford University School of Medicine, 1050 Arastradero Road, Palo Alto, California 94304, USA


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